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TNFRSF25 promotes Th2 polarization after CD28 costimulation
Author(s) -
Wolf Dietlinde,
Deyev Vadim,
Adkins Becky,
Podack Eckhard R.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1070.18
Subject(s) - cd28 , stimulation , co stimulation , microbiology and biotechnology , cytokine , effector , receptor , biology , t cell , chemistry , immunology , endocrinology , immune system , genetics
TNFRSF25 (TNFR25) is a member of the TNF‐receptor family; its ligand is TL1A (TNFSF15). TNFR25 is expressed constitutively on murine CD4 + T cells and up‐regulated after T cell activation. We have shown previously that genetic blockade of TNFR25 signals in CD4 + T cells interferes with Th2 polarization in vivo and in vitro . Investigating the molecular mechanism, we now show that CD28 co‐stimulation during primary activation causes significant up‐regulation of TNFR25 on CD4 + T cells. TNFR25 signals, elicited with an agonistic anti‐TNFR25 antibody (4C12) during secondary stimulation, mediate significant up‐regulation of Th2 cytokine production. In dominant negative (DN) TNFR25 transgenic CD4 + T cells, 4C12 does not up‐regulate Th2 cytokine production despite up‐regulation of DN‐TNFR25 and endogenous TNFR25 expression. We conclude that TNFR25 signals are supportive and may be required for up‐regulation of Th2 cytokine production during secondary stimulation of Th2 polarized effector/memory CD4 + T cells.