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Volume 272, Number 11, Issue of March 14, 1997 pp. 7314-7319
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.

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Interleukin-4 Signaling in B Lymphocytes from Patients with X-linked Severe Combined Immunodeficiency

(Received for publication, October 29, 1996, and in revised form, December 17, 1996)

Naomi Taylor ^§ , Fabio Candotti , Susan Smith , Scott A. Oakes , Thomas Jahn , Judith Isakov ^§§ , Jennifer M. Puck ^§§ , John J. O'Shea , Kenneth Weinberg and James A. Johnston

From the  Division of Research Immunology and Bone Marrow Transplantation, Childrens Hospital Los Angeles, Los Angeles, California 90027, ^§ Institut de Génétique Moléculaire de Montpellier, 34033 Montpellier, France,  Clinical Gene Therapy Branch, National Center for Human Genome Research,  Lymphocyte Cell Biology Section, NIAMSD and ^§§ Immunological Genetics Section, National Center for Human Genome Research, National Institutes of Health, Bethesda, Maryland 20855

Interleukin-4 (IL-4) is an important cytokine for B and T lymphocyte function and mediates its effects via a receptor that contains _c. B cells derived from patients with X-linked severe combined immunodeficiency (X-SCID) are deficient in _c and provide a useful model in which to dissect the role of this subunit in IL-4-mediated signaling. We found that although IL-4 stimulation of X-SCID B cells did not result in Janus tyrosine kinase-3 (JAK3) phosphorylation, other IL-4 substrates including JAK1 and IRS-1 were phosphorylated. Additionally, we detected signal transducers and activators of transcription 6 (STAT6) tyrosine phosphorylation and DNA binding activity in X-SCID B cells with a wide range of _c mutations. However, reconstitution of these X-SCID B cells with _c enhanced IL-4-mediated responses including STAT6 phosphorylation and DNA binding activity and resulted in increased CD23 expression. Thus, _c is not necessary to trigger IL-4-mediated responses in B cells, but its presence is important for optimal IL-4-signaling. These results suggest that two distinct IL-4 signaling pathways exist.

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