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Blood, 1 January 2001, Vol. 97, No. 1, pp. 221-226
IMMUNOBIOLOGY
JAB/SOCS1/SSI-1 is an interleukin-2-induced inhibitor of
IL-2 signaling
Bernhard Sporri,
Panu E. Kovanen,
Atsuo Sasaki,
Akihiko Yoshimura, and
Warren
J. Leonard
From the Laboratory of Molecular Immunology, National
Heart, Lung and Blood Institute, National Institutes of Health,
Bethesda, MD, and the Institute of Life Science, Kurume University,
Kurume, Japan.
JAB/suppressor of cytokine signaling 1 (SOCS1) STAT-induced
STAT inhibitor-1 (SSI-1) (JAB/SOCS1/SSI-1) is an
SH2-domain-containing protein that is induced by and negatively
regulates signaling by a number of cytokines including interleukin-4
(IL-4), IL-6, interferon (IFN)- , prolactin, growth hormone, and
erythropoietin. The role of JAB/SOCS1/SSI-1 in IL-2 signaling
has been analyzed. JAB/SOCS1/SSI-1 is strongly induced by IL-2 in
peripheral blood T cells, and JAB/SOCS1/SSI-1 overexpression strongly
inhibits IL-2-induced signal transducer and activator of
transcription-5 (Stat5) phosphorylation and transcriptional activity.
In cotransfection experiments, JAB/SOCS1/SSI-1 associates with both
Jak1 and Jak3; however, JAB/SOCS1/SSI-1 had a greater effect on Jak1
tyrosine phosphorylation and kinase activity. JAB/SOCS1/SSI-1 also
interacts with IL-2R , and this interaction requires the A region
(residues 313-382) of IL-2R. However, this interaction was not
essential for the inhibitory action of JAB. Thus, JAB/SOCS1/SSI-1 is an IL-2-induced inhibitor of IL-2 signaling that functions by inhibiting Jak kinase activity. This suggests an important role for
JAB/SOCS1/SSI-1 in regulating T-cell responses.
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