7,922 results match your criteria Journal of Leukocyte Biology[Journal]


Role of ADAM17 as a regulatory checkpoint of CD16A in NK cells and as a potential target for cancer immunotherapy.

J Leukoc Biol 2019 Feb 20. Epub 2019 Feb 20.

Department of Veterinary and Biomedical Sciences, University of Minnesota, St. Paul, Minnesota, USA.

Human NK cell antitumor activities involve Ab-dependent cell-mediated cytotoxicity (ADCC), which is a key mechanism of action for several clinically successful tumor-targeting therapeutic mAbs. Human NK cells exclusively recognize these Abs by the Fcγ receptor CD16A (FcγRIIIA), one of their most potent activating receptors. Unlike other activating receptors on NK cells, CD16A undergoes a rapid down-regulation in expression by a proteolytic process following NK cell activation with various stimuli. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.2MR1218-501RDOI Listing
February 2019

Human liver-derived CXCR6 NK cells are predominantly educated through NKG2A and show reduced cytokine production.

J Leukoc Biol 2019 Feb 19. Epub 2019 Feb 19.

Research Department Virus Immunology, Heinrich Pette Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany.

NK cells have been implicated to affect the outcome of numerous liver diseases. In particular, members of the killer-cell Ig-like receptor (KIR) family, predominantly expressed by NK cells, have been associated with the outcome of hepatitis C virus infection and clearance of hepatocellular carcinoma. Inhibitory KIRs tune NK cell function through interaction with HLA class I, a process termed education. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.1MA1118-428RDOI Listing
February 2019

Unraveling the host's immune response to infection: Seeing is believing.

J Leukoc Biol 2019 Feb 18. Epub 2019 Feb 18.

University of Calgary Department of Physiology and Pharmacology, University of Calgary, Calgary, Alberta, Canada.

It has long been appreciated that understanding the interactions between the host and the pathogens that make us sick is critical for the prevention and treatment of disease. As antibiotics become increasingly ineffective, targeting the host and specific bacterial evasion mechanisms are becoming novel therapeutic approaches. The technology used to understand host-pathogen interactions has dramatically advanced over the last century. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.4RI1218-503RDOI Listing
February 2019

HIV infection modulates IL-1β response to LPS stimulation through a TLR4-NLRP3 pathway in human liver macrophages.

J Leukoc Biol 2019 Feb 18. Epub 2019 Feb 18.

Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA.

IL-1β is an important mediator of innate inflammatory responses and has been shown to contribute to liver injury in a number of etiologies. HIV patients have increased necroinflammation and more rapid fibrosis progression in chronic liver injury compared to non-HIV-infected patients. As the resident liver macrophage is critical to the IL-1β response to microbial translocation in chronic liver disease, we aim to examine the impact of HIV-1 and LPS stimulation on the IL-1β response of the resident hepatic macrophages. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.4A1018-381RDOI Listing
February 2019

Monocyte heterogeneity and functions in cancer.

J Leukoc Biol 2019 Feb 18. Epub 2019 Feb 18.

La Jolla Institute for Allergy and Immunology, La Jolla, California, USA.

Monocytes are innate immune cells of the mononuclear phagocyte system that have emerged as important regulators of cancer development and progression. Our understanding of monocytes has advanced from viewing these cells as a homogenous population to a heterogeneous system of cells that display diverse responses to different stimuli. During cancer, different monocyte subsets perform functions that contribute to both pro- and antitumoral immunity, including phagocytosis, secretion of tumoricidal mediators, promotion of angiogenesis, remodeling of the extracellular matrix, recruitment of lymphocytes, and differentiation into tumor-associated macrophages and dendritic cells. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.4RI0818-311RDOI Listing
February 2019

Danger signals in oral cavity-related diseases.

J Leukoc Biol 2019 Feb 18. Epub 2019 Feb 18.

Department of Oral Biology, School of Dental Medicine, University at Buffalo, Buffalo, New York, USA.

The oral cavity is a unique environment containing teeth juxtaposed with soft tissues, all of which are constantly bathed in microbial products and host-derived factors. While microbial dysbiosis in the oral cavity clearly leads to oral inflammatory disease, recent advances find that endogenous danger-associated molecular patterns (DAMPs) released from oral and salivary tissue also contribute to the progression of inflammatory and autoimmune disease, respectively. In contrast, DAMPs produced during oral fungal infection actually promote the resolution of infection. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.4MIR1118-439RDOI Listing
February 2019

Tricarboxylic acid cycle metabolites in the control of macrophage activation and effector phenotypes.

J Leukoc Biol 2019 Feb 15. Epub 2019 Feb 15.

Department of Biochemistry and Molecular Genetics, University of Louisville, Louisville, Kentucky, USA.

The tricarboxylic acid (TCA) cycle is a mitochondrial metabolic hub that coordinates the metabolism of carbohydrates, proteins, and fats into carbon dioxide and ATP. At specific points in the cycle, the diversion, import, or export of TCA metabolites allows for the dynamic regulation of a variety of tissue and/or cell-specific phenotypic processes. Recent studies have identified that a number of TCA metabolites are important in controlling monocyte/macrophage phenotypes and effector functions while specific macrophage activation or polarization states functionally determine the relative utilization of each. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.3RU1218-496RDOI Listing
February 2019

Frontline Science: Induction of experimental autoimmune encephalomyelitis mobilizes Th17-promoting myeloid derived suppressor cells to the lung.

J Leukoc Biol 2019 Feb 14. Epub 2019 Feb 14.

Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

Myeloid-derived suppressor cells (MDSCs) are a diverse group of cells that are recognized for their remarkable suppressive effects on pro-inflammatory T cells. The pleiotropic nature of these cells, however, has been demonstrated by their differential effects on immune responses in different settings. Our and others' work has demonstrated suppressive effects of these cells. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.4HI0818-335RDOI Listing
February 2019
1 Read

The role of CNS macrophages in streptococcal meningoencephalitis.

J Leukoc Biol 2019 Feb 14. Epub 2019 Feb 14.

Institute for Immunodeficiency, Center for Chronic Immunodeficiency (CCI), Medical Center and Faculty of Medicine, University of Freiburg, Freiburg, Germany.

In the healthy brain, microglia and other CNS macrophages are the most abundant immune cell type. Thus, they form the natural immune cell interface with streptococci, which are the leading cause of bacterial meningitis and encephalitis in infants and young children. In homeostasis, the blood-brain barrier allows for very limited access of immune cells circulating in the periphery. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.4MR1118-419RDOI Listing
February 2019
1 Read

Activated NK cells kill hepatic stellate cells via p38/PI3K signaling in a TRAIL-involved degranulation manner.

J Leukoc Biol 2019 Feb 12. Epub 2019 Feb 12.

Institute of Translational Medicine, First Hospital, Jilin University, Changchun, Jilin, China.

NK cells are important in regulating hepatic fibrosis via their cytotoxic killing of hepatic stellate cells (HSCs). NK cells are activated by both cytokines such as IL-12 and IL-18, and innate immune stimuli such as ligation of TLRs. The secretion of IL-18 depends upon activation of the inflammasome, whereas TLRs are stimulated by microbial products. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.2A0118-031RRDOI Listing
February 2019
4.289 Impact Factor

The trafficking protein JFC1 regulates Rac1-GTP localization at the uropod controlling neutrophil chemotaxis and in vivo migration.

J Leukoc Biol 2019 Feb 12. Epub 2019 Feb 12.

Department of Molecular Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, California, USA.

Neutrophil chemotaxis is essential in responses to infection and underlies inflammation. In neutrophils, the small GTPase Rac1 has discrete functions at both the leading edge and in the retraction of the trailing structure at the cell's rear (uropod), but how Rac1 is regulated at the uropod is unknown. Here, we identified a mechanism mediated by the trafficking protein synaptotagmin-like 1 (SYTL1 or JFC1) that controls Rac1-GTP recycling from the uropod and promotes directional migration of neutrophils. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.1VMA0818-320RDOI Listing
February 2019

IFN-γ-dependent nitric oxide suppresses Brucella-induced arthritis by inhibition of inflammasome activation.

J Leukoc Biol 2019 Feb 12. Epub 2019 Feb 12.

Department of Veterinary Pathobiology, College of Veterinary Medicine, University of Missouri, Columbia, Missouri, USA.

Brucellosis, caused by the intracellular bacterial pathogen Brucella, is a globally important zoonotic disease for which arthritis is the most common focal complication in humans. Wild-type mice infected systemically with Brucella typically do not exhibit arthritis, but mice lacking IFN-γ develop arthritis regardless of the route of Brucella infection. Here, we investigated mechanisms by which IFN-γ suppresses Brucella-induced arthritis. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.4MIA1018-409RDOI Listing
February 2019
2 Reads

Mapping mononuclear phagocytes in blood, lungs, and lymph nodes of sarcoidosis patients.

J Leukoc Biol 2019 Feb 11. Epub 2019 Feb 11.

Division of Immunology and Allergy, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.

Sarcoidosis is a T-cell driven inflammatory disease characterized by granuloma formation. Mononuclear phagocytes (MNPs)-macrophages, monocytes, and dendritic cells (DCs)-are likely critical in sarcoidosis as they initiate and maintain T cell activation and contribute to granuloma formation by cytokine production. Granulomas manifest primarily in lungs and lung-draining lymph nodes (LLNs) but these compartments are less studied compared to blood and bronchoalveolar lavage (BAL). Read More

View Article

Download full-text PDF

Source
http://doi.wiley.com/10.1002/JLB.5A0718-280RR
Publisher Site
http://dx.doi.org/10.1002/JLB.5A0718-280RRDOI Listing
February 2019
3 Reads

Adaptive NK cell responses in HIV/SIV infections: A roadmap to cell-based therapeutics?

J Leukoc Biol 2019 Feb 7. Epub 2019 Feb 7.

Center for Virology and Vaccine Research (CVVR), Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.

NK cells play a critical role in antiviral and antitumor responses. Although current NK cell immune therapies have focused primarily on cancer biology, many of these advances can be readily applied to target HIV/simian immunodeficiency virus (SIV)-infected cells. Promising developments include recent reports that CAR NK cells are capable of targeted responses while producing less off-target and toxic side effects than are associated with CAR T cell therapies. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.MR0718-303RDOI Listing
February 2019

Microglia in Alzheimer's disease: A target for immunotherapy.

J Leukoc Biol 2019 Feb 6. Epub 2019 Feb 6.

Department of Pathology and Immunology, Washington University School of Medicine, Saint Louis, Missouri, USA.

Microglia are resident Mϕs of the CNS that play pleiotropic functions in brain development and homeostasis. Impaired microglial functions are thought to be involved in the onset and progression of various neurodevelopmental and neurodegenerative diseases. Thus, understanding microglia in these settings may indicate new approaches for therapeutic intervention. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.MR0818-319RDOI Listing
February 2019
2 Reads

Inflammasome activation: Neutrophils go their own way.

J Leukoc Biol 2019 Feb 5. Epub 2019 Feb 5.

Cochin Institute, INSERM U1016, CNRS UMR 8104, Paris Descartes University, Paris, France.

Discussion on a new RIPK3-dependent pathway to cell death and cytokine secretion independent of the canonical necroptosis and inflammasome machinery in neutrophils. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.3CE1118-433RDOI Listing
February 2019

The emerging roles of macrophages in cancer metastasis and response to chemotherapy.

J Leukoc Biol 2019 Feb 5. Epub 2019 Feb 5.

Department of Anatomy and Structural Biology, Albert Einstein College of Medicine, Bronx, New York, USA.

Macrophages represent a heterogeneous group of cells, capable of carrying out distinct functions in a variety of organs and tissues. Even within individual tissues, their functions can vary with location. Tumor-associated macrophages (TAMs) specialize into three major subtypes that carry out multiple tasks simultaneously. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.MR0218-056RRDOI Listing
February 2019

Frontline Science: TNF-α and GM-CSF1 priming augments the role of SOS1/2 in driving activation of Ras, PI3K-γ, and neutrophil proinflammatory responses.

J Leukoc Biol 2019 Feb 5. Epub 2019 Feb 5.

Inositide Laboratory, The Babraham Institute, Cambridge, UK.

Circulating neutrophils are, by necessity, quiescent and relatively unresponsive to acute stimuli. In regions of inflammation, mediators can prime neutrophils to react to acute stimuli with stronger proinflammatory, pathogen-killing responses. In neutrophils G protein-coupled receptor (GPCR)-driven proinflammatory responses, such as reactive oxygen species (ROS) formation and accumulation of the key intracellular messenger phosphatidylinositol (3,4,5)-trisphosphate (PIP ), are highly dependent on PI3K-γ, a Ras-GTP, and Gβγ coincidence detector. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.2HI0918-359RRDOI Listing
February 2019
1 Read

Lymphocyte mechanotransduction: The regulatory role of cytoskeletal dynamics in signaling cascades and effector functions.

J Leukoc Biol 2019 Feb 1. Epub 2019 Feb 1.

Laboratory of Molecular and Applied Immunology, Bar-Ilan University, The Mina and Everard Goodman Faculty of Life Sciences, Ramat-Gan, Israel.

The process of mechanotransduction, that is, conversion of physical forces into biochemical signaling cascades, has attracted interest as a potential mechanism for regulating immune cell activation. The cytoskeleton serves a critical role in a variety of lymphocyte functions, from cellular activation, proliferation, adhesion, and migration, to creation of stable immune synapses, and execution of functions such as directed cytotoxicity. Though traditionally considered a scaffold that enables formation of signaling complexes that maintain stable immune synapses, the cytoskeleton was additionally shown to play a dynamic role in lymphocyte signaling cascades by sensing physical cues such as substrate rigidity, and transducing these mechanical features into chemical signals that ultimately influence lymphocyte effector functions. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.MR0718-267RDOI Listing
February 2019

Progress and history of the 10th Federation of African Immunological Societies Congress.

J Leukoc Biol 2019 Feb;105(2):229-232

Department of Immunology, Institut Pasteur de Tunis and University Tunis El Manar, Tunis, Tunisia.

The 10th Federation of African Immunological Societies (FAIS) Congress, held in Tunisia in November 2017, marked a significant scientific milestone. It enabled scientists from across the continent to promote immunology research and to showcase major achievements made by immunologists throughout Africa. This issue of the Journal of Leukocyte Biology (JLB) features manuscripts from the FAIS Congress. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.5MR1218-493DOI Listing
February 2019

Leukemia-derived exosomes and cytokines pave the way for entry into the brain.

J Leukoc Biol 2019 Jan 31. Epub 2019 Jan 31.

Department of Pathology, University of New Mexico, Albuquerque, New Mexico, USA.

Infiltration of acute lymphoblastic leukemia (ALL) blasts into the CNS remains as a major clinical problem, with high risk for chemotherapy-resistant relapse and treatment-related morbidity. Despite the common inclusion of CNS prophylaxis treatments in therapy regimens, there are significant gaps in understanding the mechanisms that mediate leukemia cell entry into the CNS as well as roles for resident cells in the brain. In this study, we employ a xenograft model of human B cell precursor (BCP)-ALL in immunocompromised mice. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.3A0218-054RDOI Listing
January 2019
1 Read

OMIC signatures to understand cancer immunosurveillance and immunoediting: Melanoma and immune cells interplay in immunotherapy.

J Leukoc Biol 2019 Jan 30. Epub 2019 Jan 30.

Unidad de Investigación en Virología y Cáncer, Hospital Infantil de México Federico Gómez, Ciudad de México, México.

Melanoma is the deadliest form of skin cancer. Cutaneous melanomas usually originate from exposure to the mutagenic effects of ultraviolet radiation, and as such they exhibit the highest rate of somatic mutations than any other human cancer, and an extensive expression of neoantigens concurrently with a dense infiltrate of immune cells. The coexistence of high immunogenicity and high immune cell infiltration may sound contradictory for cancers carrying a gloomy outcome. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.MR0618-241RRDOI Listing
January 2019
1 Read

Differential contribution of education through KIR2DL1, KIR2DL3, and KIR3DL1 to antibody-dependent (AD) NK cell activation and ADCC.

J Leukoc Biol 2019 Jan 30. Epub 2019 Jan 30.

Research Institute of the McGill University Health Center (RI-MUHC), Montreal, Quebec, Canada.

The engagement of activating NK receptors (aNKR) stimulates NK cell activity, provided that interactions between inhibitory NK receptors (iNKR) with their HLA ligands do not override them. Abs bound to target cells can also activate NK cells by engaging the CD16 aNKR. NK cell education status is an important factor for Ab-dependent NK cell activation (ADNKA) of some NK cell subsets. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.4A0617-242RRRDOI Listing
January 2019
2 Reads

Mitochondria as emerging targets for therapies against T cell acute lymphoblastic leukemia.

J Leukoc Biol 2019 Jan 30. Epub 2019 Jan 30.

Laboratory of Immunobiology and Ionic Transport Regulation, University Center for Biomedical Research, University of Colima, Colima, Mexico.

Acute lymphoblastic leukemia (ALL) comprises a heterogeneous group of hematologic malignancies, arising from diverse genetic alterations in the early lymphocyte development. T-cell subtype of ALL (T-ALL) accounts for about 15% and 25% of ALL in children and adults, respectively. Being less frequent among ALL subtypes, T-ALL represents a high-risk factor for poor prognosis due to its aggressiveness and resistance to common antileukemic drugs. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.5VMR0818-330RRDOI Listing
January 2019

Interleukin-5 induces apoptotic defects in CD4 T cells of patients with allergic rhinitis.

J Leukoc Biol 2019 Jan 29. Epub 2019 Jan 29.

Research Center of Allergy & Immunology, Shenzhen University School of Medicine, Shenzhen, China.

T helper (Th)2 polarization plays an important role in the pathogenesis of allergic diseases; the underlying mechanism remains to be further investigated. B cell lymphoma protein-2 like protein-12 (Bcl2L12) has the anti-apoptotic function. This study aims to elucidate the contribution of Bcl2L12 to Th2 polarization in patients with allergic rhinitis (AR). Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.3A0718-287RRDOI Listing
January 2019
2 Reads

Detecting lipopolysaccharide in the cytosol of mammalian cells: Lessons from MD-2/TLR4.

J Leukoc Biol 2019 Jan 29. Epub 2019 Jan 29.

Inflammation Program and the Departments of Internal Medicine and Microbiology, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA.

Proinflammatory immune responses to Gram-negative bacterial lipopolysaccharides (LPS) are crucial to innate host defenses but can also contribute to pathology. How host cells sensitively detect structural features of LPS was a mystery for years, especially given that a portion of the molecule essential for its potent proinflammatory properties-lipid A-is buried in the bacterial membrane. Studies of responses to extracellular and vacuolar LPS revealed a crucial role for accessory proteins that specifically bind LPS-rich membranes and extract LPS monomers to generate a complex of LPS, MD-2, and TLR4. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.3MIR1118-434RDOI Listing
January 2019
1 Read

Loss of RHBDF2 results in an early-onset spontaneous murine colitis.

J Leukoc Biol 2019 Jan 29. Epub 2019 Jan 29.

Inflammation Program, Roy J. and Lucille A. Carver College of Medicine University of Iowa, Iowa City, Iowa, USA.

Inflammatory bowel disease (IBD) is a heterogeneous group of inflammation-mediated pathologies that include Crohn's disease and ulcerative colitis and primarily affects the colon and small intestine. Previous studies have shown that a disintegrin and metalloprotease (ADAM) 17, a membrane-bound sheddase, capable of cleaving the proinflammatory cytokine TNF and epidermal growth factor receptor ligands, plays a critical role in maintaining gut homeostasis and modulating intestinal inflammation during IBD. Rhomboid 5 homolog 2 (RHBDF2), a catalytically inactive member of the rhomboid family of intramembrane serine proteases, was recently identified as a crucial regulator of ADAM17. Read More

View Article

Download full-text PDF

Source
http://doi.wiley.com/10.1002/JLB.4A0718-283RR
Publisher Site
http://dx.doi.org/10.1002/JLB.4A0718-283RRDOI Listing
January 2019
5 Reads
4.289 Impact Factor

Frontline Science: Employing enzymatic treatment options for management of ocular biofilm-based infections.

J Leukoc Biol 2019 Jan 28. Epub 2019 Jan 28.

Department of Medicine, Division of Infectious Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.

Pseudomonas aeruginosa-induced corneal keratitis is a sight-threatening disease. The rise of antibiotic resistance among P. aeruginosa keratitis isolates makes treatment of this disease challenging, emphasizing the need for alternative therapeutic modalities. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.4HI0918-364RRDOI Listing
January 2019

Tissue-type plasminogen activator neutralizes LPS but not protease-activated receptor-mediated inflammatory responses to plasmin.

J Leukoc Biol 2019 Jan 28. Epub 2019 Jan 28.

The Department of Pathology, University of California San Diego, La Jolla, California.

Tissue-type plasminogen activator (tPA) activates fibrinolysis and also suppresses innate immune system responses to LPS in bone marrow-derived macrophages (BMDMs) and in vivo in mice. The objective of this study was to assess the activity of tPA as a regulator of macrophage physiology in the presence of plasmin. Enzymatically active and enzymatically inactive (EI) tPA appeared to comprehensively block the response to LPS in BMDMs, including expression of proinflammatory cytokines such as TNF-α and IL-1β and anti-inflammatory cytokines such as IL-10 and IL-1 receptor antagonist. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.3A0818-329RRRDOI Listing
January 2019
1 Read

20-Hydroxy- and 20-carboxy-leukotriene (LT) B downregulate LTB -mediated responses of human neutrophils and eosinophils.

J Leukoc Biol 2019 Jan 24. Epub 2019 Jan 24.

Centre de recherche de l'Institut universitaire de cardiologie et pneumologie de Québec-Université Laval, Département de médecine, Faculté de médecine, Université Laval, Québec City, QC, G1V 4G5, Canada.

Leukotriene B (LTB ) plays a prominent role in innate immunity as it induces phagocyte recruitment, the release of antimicrobial effectors, and as it potentiates the ingestion and killing of pathogens. In humans, LTB has a short half-life and is rapidly metabolized by leukocytes, notably into 20-OH- and 20-COOH-LTB by neutrophils. Although these LTB metabolites bind to the BLT receptor with high affinity, they activate neutrophils to a much lower extent than LTB . Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.MA0718-306RDOI Listing
January 2019

NK cell metabolism.

Authors:
Clair M Gardiner

J Leukoc Biol 2019 Jan 24. Epub 2019 Jan 24.

School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin 2, Ireland.

Natural Killer (NK) cells are important antiviral and anticancer effector cells. They have excellent potential for immunotherapy although impaired functions during cancer limit their effectiveness. The discovery that cellular metabolism can impact on and regulate immune functions has led to an explosion of articles in this new area of immunometabolism. Read More

View Article

Download full-text PDF

Source
http://doi.wiley.com/10.1002/JLB.MR0718-260R
Publisher Site
http://dx.doi.org/10.1002/JLB.MR0718-260RDOI Listing
January 2019
6 Reads

The multiple faces of CD5.

J Leukoc Biol 2019 Jan 24. Epub 2019 Jan 24.

Department of Immunology, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, México City, México.

Since its discovery, over 30 years ago, CD5 has been used as a marker to identify T cells, B1-a cells, and B cell chronic lymphocytic leukemia cells. Throughout the years, many studies have described the functional relevance of CD5 as a modulator of T and B cell receptor signaling. However, it has not been until recent years that CD5 has emerged as a functional receptor in other areas of the immune system. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.MR0618-226RDOI Listing
January 2019
1 Read

TREM-1 regulates neutrophil chemotaxis by promoting NOX-dependent superoxide production.

J Leukoc Biol 2019 Jan 22. Epub 2019 Jan 22.

Department of Internal Medicine, University of Iowa Carver College of Medicine, Iowa City, Iowa, USA.

Neutrophil migration across tissue barriers to the site of injury involves integration of complex danger signals and is critical for host survival. Numerous studies demonstrate that these environmental signals fundamentally alter the responses of extravasated or "primed" neutrophils. Triggering receptor expressed on myeloid cells 1 (TREM-1) plays a central role in modulating inflammatory signaling and neutrophil migration into the alveolar airspace. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.3VMA0918-375RDOI Listing
January 2019

Beyond the antibody: B cells as a target for bacterial infection.

J Leukoc Biol 2019 Jan 18. Epub 2019 Jan 18.

Departamento de Biomedicina Molecular, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Mexico City, Mexico.

It is well established that B cells play an important role during infections beyond antibody production. B cells produce cytokines and are APCs for T cells. Recently, it has become clear that several pathogenic bacterial genera, such as Salmonella, Brucella, Mycobacterium, Listeria, Francisella, Moraxella, and Helicobacter, have evolved mechanisms such as micropinocytosis induction, inflammasome down-regulation, inhibitory molecule expression, apoptosis induction, and anti-inflammatory cytokine secretion to manipulate B cell functions influencing immune responses. Read More

View Article

Download full-text PDF

Source
http://doi.wiley.com/10.1002/JLB.MR0618-225R
Publisher Site
http://dx.doi.org/10.1002/JLB.MR0618-225RDOI Listing
January 2019
4 Reads

The mannose 6-phosphate/insulin-like growth factor 2 receptor mediates plasminogen-induced efferocytosis.

J Leukoc Biol 2019 Jan 18. Epub 2019 Jan 18.

Molecular Immunology Unit, Institute for Hygiene and Applied Immunology, Centre for Pathophysiology, Infectiology & Immunology, Medical University of Vienna, Vienna, Austria.

The plasminogen system is harnessed in a wide variety of physiological processes, such as fibrinolysis, cell migration, or efferocytosis; and accordingly, it is essential upon inflammation, tissue remodeling, wound healing, and for homeostatic maintenance in general. Previously, we identified a plasminogen receptor in the mannose 6-phosphate/insulin-like growth factor 2 receptor (M6P/IGF2R, CD222). Here, we demonstrate by means of genetic knockdown, knockout, and rescue approaches combined with functional studies that M6P/IGF2R is up-regulated on the surface of macrophages, recognizes plasminogen exposed on the surface of apoptotic cells, and mediates plasminogen-induced efferocytosis. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.1AB0417-160RRDOI Listing
January 2019

The pathogenesis of tuberculous meningitis.

J Leukoc Biol 2019 Feb 15;105(2):267-280. Epub 2019 Jan 15.

The Francis Crick Institute, Midland Road, London, United Kingdom.

Tuberculosis (TB) remains a leading cause of death globally. Dissemination of TB to the brain results in the most severe form of extrapulmonary TB, tuberculous meningitis (TBM), which represents a medical emergency associated with high rates of mortality and disability. Via various mechanisms the Mycobacterium tuberculosis (M. Read More

View Article

Download full-text PDF

Source
http://doi.wiley.com/10.1002/JLB.MR0318-102R
Publisher Site
http://dx.doi.org/10.1002/JLB.MR0318-102RDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6355360PMC
February 2019
6 Reads

Megakaryocytes as immune cells.

J Leukoc Biol 2019 Jan 15. Epub 2019 Jan 15.

Department of Medicine, Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.

Platelets play well-recognized roles in inflammation, but their cell of origin-the megakaryocyte-is not typically considered an immune lineage. Megakaryocytes are large polyploid cells most commonly identified in bone marrow. Egress via sinusoids enables migration to the pulmonary capillary bed, where elaboration of platelets can continue. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.MR0718-261RRDOI Listing
January 2019

Targeting NKG2A to elucidate natural killer cell ontogenesis and to develop novel immune-therapeutic strategies in cancer therapy.

J Leukoc Biol 2019 Jan 15. Epub 2019 Jan 15.

Unit of Clinical and Experimental Immunology, Humanitas Clinical and Research Center, Rozzano, Milan, Italy.

Natural Killer (NK) cells are innate immune cells with a primary role in the immune surveillance against non-self-cells. NK cell recognition of "self" relies on the surface expression on autologous cells of MHC class I (MHC-I) molecules. Either the absence or the down-modulation of MHC-I on target cells "license" NK cells to kill threatening tumor-transformed or virally infected cells. Read More

View Article

Download full-text PDF

Source
http://doi.wiley.com/10.1002/JLB.MR0718-300R
Publisher Site
http://dx.doi.org/10.1002/JLB.MR0718-300RDOI Listing
January 2019
6 Reads

Extracellular CIRP (eCIRP) and inflammation.

J Leukoc Biol 2019 Jan 15. Epub 2019 Jan 15.

Center for Immunology and Inflammation, The Feinstein Institute for Medical Research, Manhasset, New York, USA.

Cold-inducible RNA-binding protein (CIRP) was discovered 2 decades ago while studying the mechanism of cold stress adaptation in mammals. Since then, the role of intracellular CIRP (iCIRP) as a stress-response protein has been extensively studied. Recently, extracellular CIRP (eCIRP) was discovered to also have an important role, acting as a damage-associated molecular pattern, raising critical implications for the pathobiology of inflammatory diseases. Read More

View Article

Download full-text PDF

Source
http://doi.wiley.com/10.1002/JLB.3MIR1118-443R
Publisher Site
http://dx.doi.org/10.1002/JLB.3MIR1118-443RDOI Listing
January 2019
4 Reads

Tamoxifen induces toxicity, causes autophagy, and partially reverses dexamethasone resistance in Jurkat T cells.

J Leukoc Biol 2019 Jan 15. Epub 2019 Jan 15.

University Center for Biomedical Research, University of Colima, Colima, Mexico.

Estrogens demonstrate biological activity in numerous organ systems, including the immune system, and exert their effects through estrogen receptors (ER) of two types: intracellular ERα and ERβ that activate transcriptional factors and membrane G protein-coupled ER GPER. The latter is capable to mediate fast activation of cytosolic signaling pathways, influencing transcriptional events in response to estrogens. Tamoxifen (TAM), widely used in chemotherapy of ERα-positive breast cancer, is considered as an ERα antagonist and GPER agonist. Read More

View Article

Download full-text PDF

Source
http://doi.wiley.com/10.1002/JLB.2VMA0818-328R
Publisher Site
http://dx.doi.org/10.1002/JLB.2VMA0818-328RDOI Listing
January 2019
9 Reads

Cells under stress: The mechanical environment shapes inflammasome responses to danger signals.

J Leukoc Biol 2019 Jan 15. Epub 2019 Jan 15.

Division of Infectious Diseases, Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri, USA.

Many intracellular signals, such as host danger-associated molecules and bacterial toxins during infection, elicit inflammasome activation. However, the mechanical environment in tissues may also influence the sensitivity of various inflammasomes to activation. The cellular mechanical environment is determined by the extracellular tissue stiffness, or its inverse, tissue compliance. Read More

View Article

Download full-text PDF

Source
http://doi.wiley.com/10.1002/JLB.3MIR1118-417R
Publisher Site
http://dx.doi.org/10.1002/JLB.3MIR1118-417RDOI Listing
January 2019
5 Reads

Frontline Science: Monocytes sequentially rewire metabolism and bioenergetics during an acute inflammatory response.

J Leukoc Biol 2019 Feb 11;105(2):215-228. Epub 2019 Jan 11.

Department of Internal Medicine/Molecular Medicine, Wake Forest School of Medicine, Winston-Salem, North Carolina, USA.

Metabolism directs the severe acute inflammatory reaction of monocytes to guard homeostasis. This occurs by sequentially activating anabolic immune effector mechanisms, switching to immune deactivation mechanisms and then restoring immunometabolic homeostasis. Nuclear sirtuin 1 and mitochondrial pyruvate dehydrogenase kinase metabolically drive this dynamic and are druggable targets that promote immunometabolic resolution in septic mice and increase survival. Read More

View Article

Download full-text PDF

Source
http://doi.wiley.com/10.1002/JLB.3HI0918-373R
Publisher Site
http://dx.doi.org/10.1002/JLB.3HI0918-373RDOI Listing
February 2019
7 Reads

Sepsis erodes CD8 memory T cell-protective immunity against an EBV homolog in a 2B4-dependent manner.

J Leukoc Biol 2019 Jan 9. Epub 2019 Jan 9.

Department of Surgery, Emory University School of Medicine, Atlanta, Georgia, USA.

Epstein-Barr virus (EBV) reactivation commonly occurs following sepsis, but the mechanisms underlying this are unknown. We utilized a murine EBV homolog (gHV) and the cecal ligation and puncture model of polymicrobial sepsis to study the impact of sepsis on gHV reactivation and CD8 T cell immune surveillance following a septic insult. We observed a significant increase in the frequency of gHV-infected germinal center B cells on day 7 following sepsis. Read More

View Article

Download full-text PDF

Source
http://doi.wiley.com/10.1002/JLB.4A0718-292R
Publisher Site
http://dx.doi.org/10.1002/JLB.4A0718-292RDOI Listing
January 2019
4 Reads

Metabolism drives monocytes during inflammation: What we do and do not know.

J Leukoc Biol 2019 Feb 7;105(2):211-213. Epub 2019 Jan 7.

Department of Anesthesiology, Vanderbilt University Medical Center, Nashville, TN, USA.

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.3CE1118-448RDOI Listing
February 2019

Sirtuin-1 in immunotherapy: A Janus-headed target.

J Leukoc Biol 2019 Jan 3. Epub 2019 Jan 3.

Division of Nephrology, Department of Pediatrics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA.

Sirtuin-1 (Sirt1), a member of the NAD-dependent sirtuin family of histone/protein deacetylases (HDAC), is an important target for immunotherapy due to its role in deacetylating the transcription factors Foxp3 and thymic retinoid acid receptor related orphan receptor gamma (RORγt). Sirt1 inhibition can increase Foxp3 acetylation and promote the production and functions of Foxp3 T-regulatory (Treg) cells, whereas the acetylation of RORγt decreases its transcriptional activity DNA binding and decreases the differentiation of proinflammatory Th17 cells. Pharmacologic inhibitors of Sirt1 increase allograft survival and decrease autoimmune colitis and experimental allergic encephalomyelitis. Read More

View Article

Download full-text PDF

Source
http://doi.wiley.com/10.1002/JLB.2RU1118-422R
Publisher Site
http://dx.doi.org/10.1002/JLB.2RU1118-422RDOI Listing
January 2019
7 Reads

Immunometabolism and innate immunity in the context of immunological maturation and respiratory pathogens in young children.

Authors:
David Verhoeven

J Leukoc Biol 2019 Jan 3. Epub 2019 Jan 3.

Department of Veterinary Microbiology and Preventative Medicine, Iowa State University, Ames, Iowa, USA.

Although children growing from birth into young adulthood undergo rapid physiological maturation, their immune systems are also undergoing significant changes that may affect how they respond to microbes and especially respiratory pathogens. A key component of control over microbes is the innate immune system that sustains pathogen suppression/elimination until the adaptive immune system can instigate clearance. Here, this review will summarize key characteristics of the developing innate immune system of neonates, infants, and toddlers. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.MR0518-204RRDOI Listing
January 2019

Obituary: Dr. Vito Pistoia.

J Leukoc Biol 2019 Jan 28;105(1):203. Epub 2018 Sep 28.

Department of Medical Biotechnologies and Translational Medicine, Medical School of Milan University, Milan, Italy.

View Article

Download full-text PDF

Source
http://doi.wiley.com/10.1002/JLB.5LT0918-363
Publisher Site
http://dx.doi.org/10.1002/JLB.5LT0918-363DOI Listing
January 2019
1 Read

Stressing out the mitochondria: Mechanistic insights into NLRP3 inflammasome activation.

J Leukoc Biol 2019 Feb 27;105(2):377-399. Epub 2018 Dec 27.

Hudson Institute of Medical Research, Clayton, Victoria, Australia.

Inflammasomes are multimeric protein complexes that induce the cleavage and release of bioactive IL-1β and cause a lytic form of cell death, termed pyroptosis. Due to its diverse triggers, ranging from infectious pathogens and host danger molecules to environmental irritants, the NOD-like receptor protein 3 (NLRP3) inflammasome remains the most widely studied inflammasome to date. Despite intense scrutiny, a universal mechanism for its activation remains elusive, although, recent research has focused on mitochondrial dysfunction or potassium (K ) efflux as key events. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.MR0318-124RDOI Listing
February 2019

Update on immunogenetics of Tunisian endemic pemphigus foliaceus.

J Leukoc Biol 2019 Feb 21;105(2):257-265. Epub 2018 Dec 21.

Department of Dermatology, Hedi Chaker Hospital, University of Sfax, Sfax, Tunisia.

Pemphigus foliaceus (PF) is an autoimmune blistering skin disease characterized by the presence of bullous skin lesions, the absence of mucous tissue involvement, and the production of auto-antibodies directed against a keratinocyte transmembrane protein localized in the desmosome and member of the cadherines, desmoglein 1. These pathogenic auto-antibodies are responsible for the intra-epidermal formation of blisters through the loss of keratinocyte adhesion, the so-called acantholysis process. The endemic form of PF observed in the south of Tunisia is characterized by a significantly higher incidence rate compared to the sporadic form in northern countries, occurrence mainly in young women and the absence of cases during childhood. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.MR0318-132RDOI Listing
February 2019
2 Reads

Impact of maternal HIV exposure, feeding status, and microbiome on infant cellular immunity.

J Leukoc Biol 2019 Feb 21;105(2):281-289. Epub 2018 Dec 21.

Division of Immunology, Institute of Infectious Diseases and Molecular Medicine, University of Cape Town, Cape Town, South Africa.

At least one-third of infants born in sub-Saharan Africa have been exposed to the effects of maternal HIV infection and antiretroviral treatment. Intrauterine HIV exposure is associated with increased rates of morbidity and mortality in children. Although the mechanisms responsible for poor infant health with HIV-1 exposure are likely to be multifactorial, we posit that the maternal environment during gestation and in the perinatal period results in altered infant immunity and is possibly the strongest contributing factor responsible for the disproportionally high infectious events among HIV-exposed infants who remain HIV uninfected. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1002/JLB.MR0318-120RDOI Listing
February 2019