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Functional signaling of membrane‐bound TL1A induces IFN‐γ expression
Author(s) -
Biener-Ramanujan Eva,
Gonsky Rivkah,
Ko Brian,
Targan Stephan R.
Publication year - 2010
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2010.04.030
Subject(s) - hek 293 cells , chemistry , secretion , transmembrane protein , microbiology and biotechnology , receptor , tumor necrosis factor alpha , immunology , biology , biochemistry
TL1A, a TNF member implicated in autoimmune diseases, is a transmembrane protein that is processed to release soluble TL1A (TL1A‐S). TL1A‐S induces a Th1 response, although the functional significance of membrane‐bound TL1A (TL1A‐M) remains unknown. We generated TL1A‐M expression in HEK‐293 cells capable of binding DR3‐Fc. Co‐incubating IL‐12/IL‐18‐primed CD4 + T cells with HEK‐293 cells expressing TL1A‐M induced 3‐fold increase in IFN‐γ that was blocked by anti‐TL1A Ab. These results demonstrate that TL1A‐M can bind death domain receptor 3 (DR3) through cell–cell contact to induce downstream IFN‐γ secretion enhancement. Anti‐TL1A antibodies designed to treat immune diseases should be verified to block both endogenous TL1A forms.