Dr. Abdulraouf Ramadan, Ph>D - Indiana university

Dr. Abdulraouf Ramadan

Ph>D

Indiana university

Indianapolis, Indiana | USA

Main Specialties: Other

Additional Specialties: Im,munology

Dr. Abdulraouf Ramadan, Ph>D - Indiana university

Dr. Abdulraouf Ramadan

Ph>D
Introduction

Primary Affiliation: Indiana university - Indianapolis, Indiana , USA

Specialties:

Additional Specialties:

Metrics

7

Publications

642

Profile Views

58

Reads

69

PubMed Central Citations

Top co-authors
Nathalie Thieblemont
Nathalie Thieblemont

Université Paris Descartes

2
Pierre Tiberghien
Pierre Tiberghien

Université de Franche-Comté

1
Christophe Ferrand
Christophe Ferrand

Université de Franche-Comté

1
Marina Deschamps
Marina Deschamps

Université de Franche-Comté

1
Carole Henry
Carole Henry

Saint-Denis Hospital (93)

1
Nicolas Montcuquet
Nicolas Montcuquet

Université Paris-Diderot

1
Eric Robinet
Eric Robinet

Université de Franche-Comté

1

Publications

7Publications

58Reads

69PubMed Central Citations

Various forms of tissue damage and danger signals following hematopoietic stem-cell transplantation.

Front Immunol 2015 28;6:14. Epub 2015 Jan 28.

Department of Pediatrics, Melvin and Bren Simon Cancer Center, Indiana University , Indianapolis, IN , USA ; Department of Microbiology and Immunology, Indiana University , Indianapolis, IN , USA.

View Article
February 2015
7 Reads
12 PubMed Central Citations(source)

Bispecificity for myelin and neuronal self-antigens is a common feature of CD4 T cells in C57BL/6 mice.

J Immunol 2014 Oct 18;193(7):3267-77. Epub 2014 Aug 18.

INSERM, U1043, Toulouse F-31300, France; Centre National de la Recherche Scientifique, U5282, Toulouse F-31300, France; Centre de Physiopathologie Toulouse-Purpan, Université Toulouse 3, Toulouse F-31300, France; Département d'Immunologie, Centre Hospitalier Universitaire Toulouse, Hôpital Purpan, Toulouse F-31300, France

View Article
October 2014
11 Reads
4 PubMed Central Citations(source)
4.92 Impact Factor

Activation of basophils by the double-stranded RNA poly(A:U) exacerbates allergic inflammation

Allergy. 2013 Jun;68(6):732-8. doi: 10.1111/all.12151. Epub 2013 Apr 27.

Allergy.

BACKGROUND: It is commonly acknowledged that asthma is exacerbated by viral infections. On the other hand, basophil infiltration of lung tissues has been evidenced postmortem in cases of fatal disease, raising the question of a possible link between these two observations. OBJECTIVES: Herein, we addressed the relationship between asthma exacerbation by viral infection and basophil activation and expansion by investigating how stimulation with the dsRNA polyadenylic/polyuridylic acid [poly(A:U)] affected basophil activities and recruitment in an allergic airway inflammation model. METHODS: The effect of dsRNA on basophils was assessed by measuring the cytokine levels produced upon stimulation. We used an OVA-induced experimental model of allergic asthma. Airway hyperreactivity, recruitment of infiltrating cells, and cytokine production were determined in the lung of mice having received poly(A:U), as compared with untreated controls. The exacerbating effect of basophils was assessed both by adoptive transfer of poly(A:U)-treated basophils and by their in vivo depletion with Ba103 antibody. RESULTS: We found that in vitro treatment with poly(A:U) increased basophil functions by inducing TH 2-type cytokine and histamine production, whereas in vivo treatment increased peripheral basophil recruitment. Furthermore, we provide the first demonstration for increased infiltration of basophils in the lung of mice suffering from airway inflammation. In this model, disease symptoms were clearly exacerbated upon adoptive transfer of basophils exposed to poly(A:U), relative to their unstimulated counterpart. Conversely, in vivo basophil depletion alleviated disease syndromes, thus validating the transfer data. CONCLUSIONS: Our findings provide the first evidence for airway inflammation exacerbation by basophils following dsRNA stimulation.

View Article
June 2013
10 Reads

IL-33 activates unprimed murine basophils directly in vitro and induces their in vivo expansion indirectly by promoting hematopoietic growth factor production.

J Immunol. 2009 Sep 15;183(6):3591-7. doi: 10.4049/jimmunol.0900328. Epub 2009 Aug 14.

J Immunol.

IL-33, a new member of the IL-1 family, has been described as an important inducer of Th2 cytokines and mediator of inflammatory responses. In this study, we demonstrate that murine basophils sorted directly from the bone marrow, without prior exposure to IL-3 or Fc(epsilon)R cross-linking, respond to IL-33 alone by producing substantial amounts of histamine, IL-4, and IL-6. These cells express ST2 constitutively and generate a cytokine profile that differs from their IL-3-induced counterpart by a preferential production of IL-6. In vivo, IL-33 promotes basophil expansion in the bone marrow (BM) through an indirect mechanism of action depending on signaling through the beta(c) chain shared by receptors for IL-3, GM-CSF, and IL-5. IL-3 can still signal through its specific beta(IL-3) chain in these mutant mice, which implies that it is not the unique growth-promoting mediator in this setup, but requires IL-5 and/or GMCSF. Our results support a major role of the latter growth factor, which is readily generated by total BM cells as well as sorted basophils in response to IL-33 along with low amounts of IL-3. Furthermore, GM-CSF amplifies IL-3-induced differentiation of basophils from BM cells, whereas IL-5 that is also generated in vivo, affects neither their functions nor their growth in vitro or in vivo. In conclusion, our data provide the first evidence that IL-33 not only activates unprimed basophils directly, but also promotes their expansion in vivo through induction of GM-CSF and IL-3.

View Article
September 2009
9 Reads

Ginger prevents Th2-mediated immune responses in a mouse model of airway inflammation.

Int Immunopharmacol 2008 Dec 8;8(12):1626-32. Epub 2008 Aug 8.

CNRS UMR 8147, Université Paris Descartes, Faculté de Médecine, Hôpital Necker, 161 rue de Sèvres; 75783 Paris Cedex 15, France.

View Article
December 2008
26 Reads
4 PubMed Central Citations(source)
2.47 Impact Factor
Top co-authors
Nathalie Thieblemont
Nathalie Thieblemont

Université Paris Descartes

2
Pierre Tiberghien
Pierre Tiberghien

Université de Franche-Comté

1
Christophe Ferrand
Christophe Ferrand

Université de Franche-Comté

1
Marina Deschamps
Marina Deschamps

Université de Franche-Comté

1
Carole Henry
Carole Henry

Saint-Denis Hospital (93)

1
Nicolas Montcuquet
Nicolas Montcuquet

Université Paris-Diderot

1
Eric Robinet
Eric Robinet

Université de Franche-Comté

1