Publications by authors named "Mohammad Javad Mousavi"

18 Publications

  • Page 1 of 1

Association of the genetic polymorphisms in inhibiting and activating molecules of immune system with rheumatoid arthritis: A systematic review and meta-analysis.

J Res Med Sci 2021 31;26:22. Epub 2021 Mar 31.

Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Several studies have demonstrated that the genetic polymorphisms in the genes encoding immune regulatory molecules, namely cytotoxic T-lymphocyte-associated protein 4 (CTLA4) and CD28, play a fundamental role in susceptibility to rheumatoid arthritis (RA). Several disperse population studies have resulted in conflicting outcomes regarding the genetic polymorphisms in these genes and RA risk. This systematic review and meta-analysis study was performed to reach a conclusive understanding of the role of single-nucleotide polymorphisms (SNPs) of CTLA4-rs231775, CTLA4-rs5742909, and CD28-rs1980422 in susceptibility to RA. Databases (ISI Web of Science, MEDLINE/PubMed, and Scopus) were searched to find the case-control studies surveying the association of CTLA4 gene rs231775, CTLA4 gene rs5742909, and CD28 gene rs1980422 polymorphisms and RA susceptibility in different population until August 2020. Association comparison between the polymorphisms and RA proneness was assessed using pooled odds ratio (OR) and their corresponding 95% confidence interval. This study was conducted on 16 population studies, comprising 1078 RA patients and 1118 healthy controls for CTLA4-rs231775, 2193 RA patients and 2580 healthy controls for CTLA4-rs5742909, and 807 RA patients and 732 healthy controls for CD28-rs1980422. Analysis indicated that G-allele, GG and GA genotypes, and dominant model for rs231775, recessive model for rs5742909, and C-allele, CC and CT genotypes, and recessive model for rs1980422 were significantly associated with increased RA risk. This meta-analysis showed that genetic polymorphisms of both immune inhibitory and activating genes, including CTLA4-rs231775, CTLA4-rs5742909, and CD28-rs1980422 polymorphisms, may increase susceptibility to RA.
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http://dx.doi.org/10.4103/jrms.JRMS_567_20DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8240549PMC
March 2021

SARS-Cov-2 and COVID-19, Basic and Clinical Aspects of the Human Pandemic: A Review.

Iran J Public Health 2021 Apr;50(4):665-675

Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

In the last two decades, we have witnessed three major epidemics of the coronavirus human disease namely, severe acute respiratory syndrome (SARS), Middle Eastern respiratory syndrome, and more recently an ongoing global pandemic of coronavirus disease 2019 (COVID-19). Iran, a country of nearly 84 million, in the Middle East, severely involved with the COVID-19 disease. A documented multidimensional approach to COVID-19 disease is therefore mandatory to provide a well-balanced platform for the concerned medical community in our county and beyond. In this review, we highlight the disease status in Iran and attempt to provide a multilateral view of the fundamental and clinical aspects of the disease including the clinical features of the confirmed cases, virology, pathogenesis, epidemiology, and laboratory methods needed for diagnosis.
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http://dx.doi.org/10.18502/ijph.v50i4.5991DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8219633PMC
April 2021

Role of Fibroblast Activation Protein Alpha in Fibroblast-like Synoviocytes of Rheumatoid Arthritis.

Iran J Allergy Asthma Immunol 2021 Jun 6;20(3):338-349. Epub 2021 Jun 6.

Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran AND Inflammation Research Center, Tehran University of Medical Sciences, Tehran, Iran.

Fibroblast-like synoviocytes (FLSs) have been introduced in recent years as a key player in the pathogenesis of rheumatoid arthritis (RA), but the exact mechanisms of their transformation and intracellular pathways have not yet been determined. This study aimed to investigate the role of fibroblast activation protein-alpha (FAP-α) in the regulation of genes involved in the transformation and pathogenic activity of RA FLSs. Synovial FLSs were isolated from RA patients and non-arthritic individuals (n=10 in both groups) and characterized; using immunocytochemistry and flow cytometry analysis. FLSs were divided into un-treated and Talabostat-treated groups to evaluate the FAP-α effect on the selected genes involved in cell cycle regulation (p21, p53, CCND1), apoptosis (Bcl-2, PUMA), and inflammatory and destructive behavior of FLSs (IL-6, TGF-β1, MMP-2, MMP-9, P2RX7). Gene expression analysis was performed by quantitative real-time polymerase chain reaction (qRT-PCR), and immunoblotting was carried out to evaluate FAP-α protein levels. The basal level of FAP-α protein in RA patients was significantly higher than non-arthritic control individuals. However, no differences were observed between RA and non-arthritic FLSs, at the baseline mRNA levels of all the genes. Talabostat treatment significantly reduced FAP-α protein levels in both RA and non-arthritic FLSs, however, had no effect on mRNA expressions except an upregulated TGF-β1 expression in non-arthritic FLSs. A significantly higher protein level of FAP-α in FLSs of RA patients compared with that of healthy individuals may point to the pathogenic role of this protein in RA FLSs. However, more investigations are necessary to address the mechanisms mediating the FAP-α pathogenic role in RA FLSs.
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http://dx.doi.org/10.18502/ijaai.v20i3.6335DOI Listing
June 2021

Transformation of fibroblast-like synoviocytes in rheumatoid arthritis; from a friend to foe.

Auto Immun Highlights 2021 Feb 5;12(1). Epub 2021 Feb 5.

Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.

Swelling and the progressive destruction of articular cartilage are major characteristics of rheumatoid arthritis (RA), a systemic autoimmune disease that directly affects the synovial joints and often causes severe disability in the affected positions. Recent studies have shown that type B synoviocytes, which are also called fibroblast-like synoviocytes (FLSs), as the most commonly and chiefly resident cells, play a crucial role in early-onset and disease progression by producing various mediators. During the pathogenesis of RA, the FLSs' phenotype is altered, and represent invasive behavior similar to that observed in tumor conditions. Modified and stressful microenvironment by FLSs leads to the recruitment of other immune cells and, eventually, pannus formation. The origins of this cancerous phenotype stem fundamentally from the significant metabolic changes in glucose, lipids, and oxygen metabolism pathways. Moreover, the genetic abnormalities and epigenetic alterations have recently been implicated in cancer-like behaviors of RA FLSs. In this review, we will focus on the mechanisms underlying the transformation of FLSs to a cancer-like phenotype during RA. A comprehensive understanding of these mechanisms may lead to devising more effective and targeted treatment strategies.
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http://dx.doi.org/10.1186/s13317-020-00145-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7863458PMC
February 2021

Escape from X chromosome inactivation and female bias of autoimmune diseases.

Mol Med 2020 12 9;26(1):127. Epub 2020 Dec 9.

Department of Medical Laboratory Sciences, School of Allied Medical Sciences, Kashan University of Medical Sciences, Kashan, Iran.

Generally, autoimmune diseases are more prevalent in females than males. Various predisposing factors, including female sex hormones, X chromosome genes, and the microbiome have been implicated in the female bias of autoimmune diseases. During embryogenesis, one of the X chromosomes in the females is transcriptionally inactivated, in a process called X chromosome inactivation (XCI). This equalizes the impact of two X chromosomes in the females. However, some genes escape from XCI, providing a basis for the dual expression dosage of the given gene in the females. In the present review, the contribution of the escape genes to the female bias of autoimmune diseases will be discussed.
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http://dx.doi.org/10.1186/s10020-020-00256-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7727198PMC
December 2020

Interleukin 4 gene polymorphism (-589C/T) and the risk of asthma: a meta-analysis and met-regression based on 55 studies.

BMC Immunol 2020 10 21;21(1):55. Epub 2020 Oct 21.

Tuberculosis and Lung Diseases Research Center, Tabriz University of Medical sciences, Tabriz, Iran.

Background: Numerous investigations have previously evaluated the association of interleukin (IL) 4 gene polymorphisms and the risk of asthma, conferring inconsistent results. To resolve the incongruent outcomes yielded from different single studies, we conducted the most up-to-date meta-analysis of IL4 gene -589C/T (rs2243250) polymorphism and susceptibility to asthma.

Methods: A systematic literature search was performed in ISI web of science, Scopus, Medline/PubMed databases prior to September 2020, and the pooled odds ratio (OR) and their corresponding 95% CI were calculated to determine the association strength.

Results: Literature search led to retrieving of 49 publications (55 case-control studies) containing 9572 cases and 9881 controls. It was revealed that IL4 gene -589C/T polymorphism increased the risk of asthma across all genetic models, including dominant model (OR = 1.22), recessive model (OR = 1.17), allelic model (OR = 1.21), and TT vs. CC model (OR = 1.34), but not the CT vs. TT model. The subgroup analysis by age indicated that IL4 gene -589C/T polymorphism was significantly associated with asthma risk in both pediatrics and adults. Additionally, the subgroup analysis by ethnicity revealed significant association in Asian, American, and Europeans. Finally, subgroup analysis by East Asian and non-East Asian populations indicated significant associations.

Conclusions: The current meta-analysis revealed that IL4 gene -589C/T polymorphism was a susceptibility risk in both pediatrics and adults in the whole and different ethnic groups.
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http://dx.doi.org/10.1186/s12865-020-00384-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7579954PMC
October 2020

Role of glucose metabolism in aggressive phenotype of fibroblast-like synoviocytes: Latest evidence and therapeutic approaches in rheumatoid arthritis.

Int Immunopharmacol 2020 Dec 8;89(Pt A):107064. Epub 2020 Oct 8.

Department of Laboratory Sciences, Khomein University of Medical Sciences, Khomein, Iran; Department of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. Electronic address:

Glucose metabolism is considerably increased in inflamed joints of rheumatoid arthritis (RA) patients at early stages. Fibroblast-like synoviocytes (FLSs) activation and subsequent joint damage are linked with metabolic alterations, especially glucose metabolism. It has been shown that glucose metabolism is elevated in aggressive phenotype of FLS cells. In this regard, glycolytic blockers are able to reduce aggressiveness of the FLS cells resulting in decreased joint damage in various arthritis models. Besides, metabolic changes in immune and non-immune cells such as FLS can provide important targets for therapeutic intervention. Glycolytic enzymes such as hexokinase 2 (HK2), phosphofructo-2-kinase/fructose-2,6-bisphosphatase (PFKFB), and phosphoglycerate kinase (PGK) play essential roles in aggressive behavior of FLS cells. It has been documented that the HK2 enzyme is significantly upregulated in RA FLS cells, compared with osteoarthritis (OA) FLS cells. The HK2 is expressed in a few tissues and upregulated in the inflamed synovium of RA patients that makes it a potential target for RA treatment. Furthermore, HK2 has different roles in each cellular compartment, which offers another level of specificity and provides a specific target to reduce deleterious effects of inhibiting the enzyme in RA without affecting glycolysis in normal cells. Thus, targeting the HK2 enzyme might be an attractive potential selective target for arthritis therapy and safer than global glycolysis inhibition. Therefore, this review was aimed to summarize the current knowledge about glucose metabolism of FLS cells and suggest novel biomarkers, which are potential candidates for RA treatment.
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http://dx.doi.org/10.1016/j.intimp.2020.107064DOI Listing
December 2020

Fertility and infertility implications in rheumatoid arthritis; state of the art.

Inflamm Res 2020 Aug 26;69(8):721-729. Epub 2020 May 26.

Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Background: A bulk of investigations imply that women with rheumatoid arthritis (RA) deliver fewer children in comparison to healthy women.

Purpose: This review article attempts to clarify the involvement of infertility-related issues in both RA men and women. Moreover, the effect of RA disease on the fertility quality and quantity will be discussed.

Results: Declined fertility rate in RA women seems to stem from modified inflammatory settings, advanced maternal age, limited sexual activity, and adverse effects of drugs on ovarian function. Women with RA may have smaller families and seem to be slower to conceive relative to their peer women. The chance of gestation in RA women may drop due to suppressed sexual function through pain and fatigue. In addition, treatment of RA women with non-steroidal anti-inflammatory drugs (NSAIDs) may prevent ovulation and therefore hinder the conception.

Conclusions: A complex interaction between RA disease and fertility related issues is present. Despite an increase rate of infertility in RA females or males, the mechanisms involved in this outcome is still unknown. Plausible causes of the decreased fertility rate in RA patients might be due to inflammatory cytokines, suppressed sexual activity, drug treatments, mother age, personal choice, or a combination of these elements.
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http://dx.doi.org/10.1007/s00011-020-01362-wDOI Listing
August 2020

Metabolic host response and therapeutic approaches to influenza infection.

Cell Mol Biol Lett 2020 5;25:15. Epub 2020 Mar 5.

4Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.

Based on available metabolomic studies, influenza infection affects a variety of cellular metabolic pathways to ensure an optimal environment for its replication and production of viral particles. Following infection, glucose uptake and aerobic glycolysis increase in infected cells continually, which results in higher glucose consumption. The pentose phosphate shunt, as another glucose-consuming pathway, is enhanced by influenza infection to help produce more nucleotides, especially ATP. Regarding lipid species, following infection, levels of triglycerides, phospholipids, and several lipid derivatives undergo perturbations, some of which are associated with inflammatory responses. Also, mitochondrial fatty acid β-oxidation decreases significantly simultaneously with an increase in biosynthesis of fatty acids and membrane lipids. Moreover, essential amino acids are demonstrated to decline in infected tissues due to the production of large amounts of viral and cellular proteins. Immune responses against influenza infection, on the other hand, could significantly affect metabolic pathways. Mainly, interferon (IFN) production following viral infection affects cell function via alteration in amino acid synthesis, membrane composition, and lipid metabolism. Understanding metabolic alterations required for influenza virus replication has revealed novel therapeutic methods based on targeted inhibition of these cellular metabolic pathways.
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http://dx.doi.org/10.1186/s11658-020-00211-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7059726PMC
November 2020

Epigenetics in rheumatoid arthritis; fibroblast-like synoviocytes as an emerging paradigm in the pathogenesis of the disease.

Immunol Cell Biol 2020 03 26;98(3):171-186. Epub 2020 Jan 26.

Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.

Rheumatoid arthritis (RA) is characterized by immune dysfunctions and chronic inflammation that mainly affects diarthrodial joints. Genetics has long been surveyed in searching for the etiopathogenesis of the disease and partially clarified the conundrums within this context. Epigenetic alterations, such as DNA methylation, histone modifications, and noncoding RNAs, which have been considered to be involved in RA pathogenesis, likely explain the nongenetic risk factors. Epigenetic modifications may influence RA through fibroblast-like synoviocytes (FLSs). It has been shown that FLSs play an essential role in the onset and exacerbation of RA, and therefore, they may illustrate some aspects of RA pathogenesis. These cells exhibit a unique DNA methylation profile in the early stage of the disease that changes with disease progression. Histone acetylation profile in RA FLSs is disrupted through the imbalance of histone acetyltransferases and histone deacetylase activity. Furthermore, dysregulation of microRNAs (miRNAs) is immense. Most of these miRNAs have shown an aberrant expression in FLSs that are involved in proliferation and cytokine production. Besides, dysregulation of long noncoding RNAs in FLSs has been revealed and attributed to RA pathogenesis. Further investigations are needed to get a better view of epigenetic alterations and their interactions. We also discuss the role of these epigenetic alterations in RA pathogenesis and their therapeutic potential.
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http://dx.doi.org/10.1111/imcb.12311DOI Listing
March 2020

Correction to: Curcumin: a modulator of inflammatory signaling pathways in the immune system.

Inflammopharmacology 2019 Oct;27(5):901

Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran.

Unfortunately, the 4th author name was incorrectly published in the original article. The complete correct name is given below.
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http://dx.doi.org/10.1007/s10787-019-00631-3DOI Listing
October 2019

Curcumin: a modulator of inflammatory signaling pathways in the immune system.

Inflammopharmacology 2019 Oct 28;27(5):885-900. Epub 2019 May 28.

Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran.

Curcumin is a natural compound derived from the spice, turmeric, that has been extensively reported for its efficacy in controlling or treatment of several inflammatory diseases. There is a growing body of literature that recognizes the anti-inflammatory effects of curcumin in the immune system. On the other hand, the role of inflammatory signaling pathways has been highlighted in the pathogenesis of several inflammatory diseases, and signaling molecules involved in these pathways are considered as valuable targets for new treatment approaches. We aimed to provide a comprehensive overview of the modulatory effects of curcumin on inflammatory signaling pathways which leads to inhibition of inflammation in different types of immune cells and animal models. In this comprehensive review, we elaborate on how curcumin can effectively inhibit multiple signaling molecules involved in inflammation including NF-κB, JAKs/STATs, MAPKs, β-catenin, and Notch-1.
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http://dx.doi.org/10.1007/s10787-019-00607-3DOI Listing
October 2019

Strategies toward rheumatoid arthritis therapy; the old and the new.

J Cell Physiol 2019 07 7;234(7):10018-10031. Epub 2018 Dec 7.

Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Currently, medications used to treat rheumatoid arthritis (RA) are glucocorticoids (GCs) and nonsteroidal anti-inflammatory drugs (NSAIDs), predominantly used for controlling the pain and inflammation, disease-modifying antirheumatic drugs (DMARDs), administered as first-line medication for newly diagnosed RA cases, and biological therapies, used to target and inhibit specific molecules of the immune and inflammatory responses. NSAIDs and other GCs are effective in alleviating the pain, inflammation, and stiffness due to RA. DMARDs that are used for RA therapy are hydroxychloroquine, methotrexate, leflunomide, and sulfasalazine. The biological therapies, on the contrary, are chimeric anti-CD20 monoclonal antibody, rituximab, inhibitors of tumor necrosis factor-α (TNF-α) like etanercept, infliximab, and adalimumab, a recombinant inhibitor of interleukin-1 (IL-1), anakinra, and costimulation blocker, abatacept. Moreover, newly under evaluation biological therapies include new TNF-α inhibitors, JAK inhibitors, anti-interleukin-6-receptor monoclonal antibodies (mABs), and antibodies against vital molecules involved in the survival and development of functional B cells. The new strategies to treat RA has improved the course of the disease and most of the patients are successful in remission of the clinical manifestations if the diagnosis of the disease occur early. The probability of remission increase if the diagnosis happens rapidly and treat-to-target approach are implemented. In this review article, we have attempted to go through the treatment strategies for RA therapy both the routine ones and those which have been developed over the past few years and currently under investigation.
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http://dx.doi.org/10.1002/jcp.27860DOI Listing
July 2019

Influenza vaccine: Where are we and where do we go?

Rev Med Virol 2019 01 8;29(1):e2014. Epub 2018 Nov 8.

Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.

The alarming rise of morbidity and mortality caused by influenza pandemics and epidemics has drawn attention worldwide since the last few decades. This life-threatening problem necessitates the development of a safe and effective vaccine to protect against incoming pandemics. The currently available flu vaccines rely on inactivated viral particles, M2e-based vaccine, live attenuated influenza vaccine (LAIV) and virus like particle (VLP). While inactivated vaccines can only induce systemic humoral responses, LAIV and VLP vaccines stimulate both humoral and cellular immune responses. Yet, these vaccines have limited protection against newly emerging viral strains. These strains, however, can be targeted by universal vaccines consisting of conserved viral proteins such as M2e and capable of inducing cross-reactive immune response. The lack of viral genome in VLP and M2e-based vaccines addresses safety concern associated with existing attenuated vaccines. With the emergence of new recombinant viral strains each year, additional effort towards developing improved universal vaccine is warranted. Besides various types of vaccines, microRNA and exosome-based vaccines have been emerged as new types of influenza vaccines which are associated with new and effective properties. Hence, development of a new generation of vaccines could contribute to better treatment of influenza.
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http://dx.doi.org/10.1002/rmv.2014DOI Listing
January 2019

Antiapoptotic Molecule Survivin in Transplantation: Helpful or Harmful?

J Transplant 2018 1;2018:6492034. Epub 2018 Oct 1.

Molecular Immunology Research Center, Tehran University of Medical Sciences, Tehran, Iran.

Survivin, an antiapoptotic molecule from inhibitor of apoptosis protein (IAP) family, is most known for its implication in cancer as there are some efforts to apply it for diagnostic as well as therapeutic purposes in oncology. On the other hand, it could be a useful molecule to be positively targeted when trying to save tissue and promote cells viability. Since protecting the allograft from ischemia reperfusion injury and inflammation-induced damage is a considerable objective in transplantation, it is reasonable to take advantage from antiapoptotic agents like survivin in order to achieve this goal. However, survivin's potential ability to induce malignancies makes some concerns about its use in clinic. The other barrier is this molecule's involvement in lymphocytes development and proliferation which might increase the risk of graft rejection due to adaptive immune system overactivation. In this review we summarize the few studies carried out about survivin's effect on graft survival and probable advantages and disadvantages of its overexpression in transplantation.
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http://dx.doi.org/10.1155/2018/6492034DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6188762PMC
October 2018

A comprehensive review on the treatment approaches of multiple sclerosis: currently and in the future.

Inflamm Res 2019 Jan 3;68(1):25-38. Epub 2018 Sep 3.

Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Background: Multiple sclerosis (MS) is a chronic and autoimmune disease of the central nervous system (CNS), mainly characterized by inflammatory demyelination, which manifests as relapses and diffuse damage and brain volume loss, both accounting for neurodegeneration, and therefore, physical disability. MS typically affects young adults and is commonly diagnosed in the early years by acute relapses, which then followed through partial or complete remission period. The clinical course of MS is characterized as four major classifications, including relapsing-remitting (RRMS), primary progressive (PPMS), progressive relapsing (PRMS), and secondary progressive (SPMS).

Purpose: This review provides comprehensive overview of the current treatments and future innovative approaches in the treatment of MS.

Results: Currently, there is no definite cure for MS. The treatment of MS has mainly been based on the prescription of immunosuppressive and immune-modulating agents. However, a number of disease-modifying treatments (DMTs) have been designed that reduce the attack rate and delay progression and mainly target inflammation settings in these patients. Although remarkable advancements have occurred in the therapy of MS, the rate of progressive disability and early mortality is still worrisome. Recently, a monoclonal antibody (ocrelizumab) was demonstrated to be beneficial in a clinical trial of primary progressive MS. Furthermore, novel treatment strategies concentrating on the remyelination or neuroprotection are under evaluation.

Conclusions: In spite of prosperous experiences in MS therapy, the future research, hopefully, will bring substantial improvements in the understanding and approaches of MS therapy.
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http://dx.doi.org/10.1007/s00011-018-1185-0DOI Listing
January 2019

Implications of the noncoding RNAs in rheumatoid arthritis pathogenesis.

J Cell Physiol 2018 01 1;234(1):335-347. Epub 2018 Aug 1.

Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.

Epigenetics refers to a set of regulatory mechanisms that affect gene expression, while the original sequence of the DNA remains unchanged. Because the advance of noncoding RNAs (ncRNAs), the role of microRNAs (miRNAs) has been gradually highlighted in the regulation of numerous cellular processes. A bulk of studies has identified that ncRNAs might be divided into several subtypes. On the one hand, investigations have disclosed the role of these molecules in normal physiological conditions of the cells. On the other hand, there is sufficient evidence that ncRNAs participate in the pathogenesis of diseases. Through this review article, we attempted to gain a comprehensive understanding of the role of ncRNAs, long ncRNAs, miRNAs, and other subtypes in pathogenesis, diagnosis, and treatment of rheumatoid arthritis (RA). Research demonstrated aberrant expression of several miRNAs in various cell and tissue types of patients with RA in comparison to the healthy individuals as well as in animal studies. Furthermore, plausible molecular mechanisms of alterations in ncRNAs expression has been discussed in causing the disease state. These alterations seem promising to be used as biomarkers in RA diagnosis. Alternately, they might be targeted by drugs to interrupt inflammation and other disease complications to treat patients with RA.
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http://dx.doi.org/10.1002/jcp.26911DOI Listing
January 2018

Toll-Like Receptor 4 in Renal Transplant.

Exp Clin Transplant 2018 06;16(3):245-252

>From the Molecular Immunology Research Center, Tehran University of Medical Sciences, Tehran, Iran.

Toll-like receptor 4 is a member of the cell surface pattern recognition receptors involved in pathogenesis of several infectious and autoimmune diseases. The wide range of Toll-like receptor 4 extrinsic and intrinsic ligands means that it has considerable ability to trigger infectious and sterile inflammation, the latter assumed to be the principal cause of ischemia-reperfusion injury. With the rising number of renal transplant procedures using deceased donors, in addition to prolonged ischemia time due to organ transport and consequently increased risk of ischemia-induced injuries, the prevention of detrimental immune responses and/or overcoming these after they initiate could be beneficial for graft survival. This review aims to summarize past and present studies conducted about the role of Toll-like receptor 4 in early and late phases of transplant, including gene expression and polymorphism evaluations.
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June 2018
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