Raif S. Geha

ORCID: 0000-0002-6019-3751
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About
Contact & Profiles
Research Areas
  • Immunodeficiency and Autoimmune Disorders
  • Immune Cell Function and Interaction
  • T-cell and B-cell Immunology
  • Dermatology and Skin Diseases
  • Asthma and respiratory diseases
  • Monoclonal and Polyclonal Antibodies Research
  • Immune Response and Inflammation
  • Cell Adhesion Molecules Research
  • Blood disorders and treatments
  • NF-κB Signaling Pathways
  • Allergic Rhinitis and Sensitization
  • Immunotherapy and Immune Responses
  • Cellular Mechanics and Interactions
  • IL-33, ST2, and ILC Pathways
  • Urticaria and Related Conditions
  • Mast cells and histamine
  • Glycosylation and Glycoproteins Research
  • Food Allergy and Anaphylaxis Research
  • Chronic Lymphocytic Leukemia Research
  • Toxin Mechanisms and Immunotoxins
  • Diabetes and associated disorders
  • Platelet Disorders and Treatments
  • Cystic Fibrosis Research Advances
  • Pediatric health and respiratory diseases
  • Cytomegalovirus and herpesvirus research

Boston Children's Hospital
2015-2024

Harvard University
2015-2024

Boston Children's Museum
2013-2024

Clinical Research Center Kiel
2016-2023

University of Leicester
2022-2023

Elliot Hospital
2022-2023

Délégation Paris 6
2022-2023

Mansoura University
2023

National Sagamihara Hospital
2019-2021

Ministry of Culture
2019-2021

Our understanding of the pathogenesis atopic dermatitis (AD) and its relationship to asthma remains incomplete. Herein, we describe a murine model epicutaneous (EC) sensitization protein allergen, chicken egg albumin, ovalbumin (OVA), which results in rise total OVA-specific serum IgE leads development characterized by infiltration CD3(+) T cells, eosinophils, neutrophils local expression mRNA for cytokines IL-4, IL-5, interferon-gamma. A single exposure EC sensitized mice aerosolized OVA...

10.1172/jci1647 article EN Journal of Clinical Investigation 1998-04-15

The tumor necrosis factor family members BAFF and APRIL induce Ig isotype switching in human B cells. We analyzed the ability of to murine cells IgG1, IgA, IgE. each engage two receptors, transmembrane activator calcium-modulator cytophilin ligand interactor (TACI) cell maturation antigen (BCMA), on In addition, engages a third receptor cells, BAFF-R. To determine role these receptors switching, we examined from mice deficient TACI, BCMA, results obtained indicate that both TACI BAFF-R are...

10.1084/jem.20032000 article EN The Journal of Experimental Medicine 2005-01-03

The X-linked hyper-IgM (XHIGM) syndrome is an uncommon primary immunodeficiency disease caused by mutations in the gene for CD40 ligand and characterized normal or elevated serum IgM, reduced levels of IgG IgA, defective T-cell function. Because its rarity, it has been difficult any single investigator institution to develop a comprehensive clinical picture this disorder. Accordingly, national registry was developed United States provide demographic, genetic, immunologic, information on...

10.1097/01.md.0000100046.06009.b0 article EN Medicine 2003-11-01

A novel pathway of IgE-B cell differentiation has been identified. Engagement the B antigen CD40 by F(ab')2 fragments monoclonal antibody (mAb) 626.1 in presence recombinant interleukin 4 (rIL-4) induced intense IgE synthesis, but modest IgG highly purified human cells. Surface IgE- cells isolated sorting were to produce mAb and IL-4. Thus, synthesis is unlikely result from expansion a population precommitted vivo. neutralizing anti-IL-6 strongly, not completely, inhibited response. This...

10.1084/jem.172.6.1861 article EN The Journal of Experimental Medicine 1990-12-01

Abstract Memory B (BMEM) cells and long-lived bone marrow plasma (BM-PCs) persist within local environmental survival niches that afford cellular longevity. However, the factors supporting BMEM cell secondary lymphoid organs allowing BM-PC persistence in remain poorly characterized. We report herein function are completely independent of BAFF (B cell-activating factor TNF family) or APRIL (a proliferation-inducing ligand). Thus, represent only mature B2 lineage subset whose is these ligands....

10.4049/jimmunol.180.6.3655 article EN The Journal of Immunology 2008-03-15

The tumor necrosis factor (TNF) family member APRIL binds to the receptors BCMA on B cells and TACI T cells. To investigate role of in immunity, we generated APRIL-deficient mice. -/- mice have normal lymphocyte development, cell proliferation vitro , but increased numbers CD44 hi CD62L lo CD4 + effector/memory IgG responses T-dependent antigens. Serum IgA levels were significantly decreased, serum antibody mucosal immunization with TD antigens type 1 T-independent impaired by itself induced...

10.1073/pnas.0307348101 article EN Proceedings of the National Academy of Sciences 2004-02-26

Autosomal recessive interleukin-1 receptor-associated kinase (IRAK)-4 and myeloid differentiation factor (MyD)88 deficiencies impair Toll-like receptor (TLR)- receptor-mediated immunity. We documented the clinical features outcome of 48 patients with IRAK-4 deficiency 12 MyD88 deficiency, from 37 kindreds in 15 countries. The were indistinguishable. There no severe viral, parasitic, fungal diseases, range bacterial infections was narrow. Noninvasive occurred 52 patients, a high incidence...

10.1097/md.0b013e3181fd8ec3 article EN Medicine 2010-11-01

Wiskott-Aldrich syndrome (WAS) is an X-linked immunodeficiency caused by mutations that affect the WAS protein (WASP) and characterized cytoskeletal abnormalities in hematopoietic cells. By using yeast two-hybrid system we have identified a proline-rich WASP-interacting (WIP), which coimmunoprecipitated with WASP from lymphocytes. WIP binds to at site distinct Cdc42 binding has actin as well profilin motifs. Expression of human B cells, but not truncation mutant lacks motif, increased...

10.1073/pnas.94.26.14671 article EN Proceedings of the National Academy of Sciences 1997-12-23

10.1016/j.jaci.2018.02.055 article EN publisher-specific-oa Journal of Allergy and Clinical Immunology 2018-05-04

B lymphocytes from patients with X chromosome-linked immunoglobulin deficiency normal or elevated serum IgM are unable to switch the synthesis of IgM/IgD that other isotypes. Isotype recombination was evaluated in three affected males by examining interleukin 4-driven IgE synthesis. T-cell-dependent completely absent patients. In contrast, CD40 mAb plus 4 induced patients' cells synthesize and undergo deletional recombination. Because interaction between its ligand on activated T is critical...

10.1073/pnas.90.6.2170 article EN Proceedings of the National Academy of Sciences 1993-03-15

The induction of IgE synthesis by IL-4 requires T cells and monocytes, as well cell- monocyte-derived cytokines. Optimal cytokine combinations, however, fail to induce highly purified B secrete IgE, indicating that additional signals are required. We show herein the human rIL-4 cognate interaction between cell receptor/CD3 complex on MHC class II antigens cells: mAbs directed against these molecules completely blocked IL-4-dependent induction. adhesion (CD2, CD4, LFA-1) also inhibited...

10.1084/jem.169.4.1295 article EN The Journal of Experimental Medicine 1989-04-01
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