Affiliation:
1. From the Division of Immunology, Children's Hospital, Harvard Medical School, Boston, MA; the Division of Allergy and Immunology, the Department of Pediatrics, Duke University Medical Center, Durham, NC; Laboratoire d'Immunogenetique Moleculaire, UMR 5535 CNRS-University, Montpellier, France; and Universite Saint-Joseph, Beirut, Lebanon.
Abstract
Abstract
CD40 is a member of the tumor necrosis factor receptor family and plays an important role in B-cell survival, growth, differentiation, and isotype switching. Recently, CD40 has been shown to associate with JAK3, a member of the family of Janus Kinases, which are nonreceptor protein kinases involved in intracellular signaling mediated by cytokines and growth factors. To investigate the role of JAK3 in CD40-mediated signaling, we studied the effect of CD40 stimulation on B-cell proliferation, IgE isotype switching, and upregulation of surface expression of CD23, ICAM-1, CD80, and LT-α in JAK3-deficient patients. Our studies show that stimulation of B cells with monoclonal antibody to CD40 in the presence of interleukin-4 (IL-4) or IL-13 resulted in similar responses in JAK3-deficient patients and normal controls. This suggests that JAK3 is not essential for CD40-mediated B-cell proliferation, isotype switching, and upregulation of CD23, ICAM-1, CD80, and LT-α surface expression.
Publisher
American Society of Hematology
Subject
Cell Biology,Hematology,Immunology,Biochemistry
Cited by
23 articles.
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