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Blood, Vol. 92 No. 7 (October 1), 1998:
pp. 2435-2440
Role of JAK3 in CD40-Mediated Signaling
Haifa H. Jabara,
Rebecca H. Buckley,
Joseph L. Roberts,
Gerard Lefranc,
Jacques Loiselet,
Georges Khalil, and
Raif S. Geha
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.
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- 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- surface expression.
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