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* Committee on Immunology and
Department of Medicine, Section of Rheumatology, University of Chicago, Chicago, IL 60637;
Department of Microbiology and Immunology, University of Miami, Miami, FL 33101; and
Department of Microbiology and Immunology, Vanderbilt University Medical School, Nashville, TN 37232
Initiation of T lymphocyte responses to most Ags requires
concurrent stimulation through the TCR and costimulatory receptors such
as CD28. Following initial activation, secondary receptors are
up-regulated that can costimulate T cells in concert with TCR
engagement. One such receptor is the TNFR family member CD30. In this
study, we report that unlike CD28, ligation of CD30 on normal effector
T cells induces IL-13 production in the absence of concurrent TCR
engagement. TCR-independent CD30-mediated IL-13 release correlated with
activation of c-Jun N-terminal kinase, p38 mitogen-activated protein
kinase (MAPK), and NF-
B, and was completely inhibited by the
expression of a TNFR-associated factor 2 (TRAF2) dominant-negative
transgene (TRAF2.DN-Tg), but not by that of an I-B
dominant-negative transgene. In parallel, expression of the TRAF2.DN-Tg
selectively prevented the induction of c-Jun N-terminal kinase and p38
MAPK, but not that of NF-B. Furthermore, IL-13 production was
reduced in a dose-dependent manner by the p38 MAPK inhibitor SB203580.
Together, these results suggest that TCR-independent CD30-mediated
production of IL-13 is triggered by association of CD30 with TRAF
family members and subsequent activation of p38 MAPK. Inasmuch as IL-13
can promote airway inflammation and cancer progression, production of
IL-13 in a TCR-independent manner has important pathological
implications in vivo.
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