Premium
DcR3/TR6 modulates immune cell interactions
Author(s) -
Wan Xiaochun,
Shi Guixiu,
Semenuk Mark,
Zhang Jun,
Wu Jiangping
Publication year - 2003
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.10523
Subject(s) - microbiology and biotechnology , immune system , peripheral blood mononuclear cell , t cell , cell , biology , cytotoxic t cell , immunology , in vitro , biochemistry
DcR3/TR6, a secreted protein, is a member of TNF receptor family. Its ligands include FasL, LIGHT, and TL1A, all TNF family members. TR6 can interfere with FasL‐ or LTβR‐mediated apoptosis; it can also inhibit T‐cell costimulation by blocking the two‐way signaling between TR2 and LIGHT, and the one‐way signaling from TL1A to DR3. In this study, we discovered that TR6 was secreted by peripheral blood mononuclear cells (PBMC) stimulated by T‐cell mitogens. It inhibited actin polymerization of T cells upon mitogen stimulation, and repress T‐cell pseudopodium formation, which is known to be important for cell–cell interaction. As a consequence, T‐cell aggregation stimulated by alloantigens, anti‐CD3 or PHA was suppressed by either soluble or solid phase TR6‐Fc. This result suggests that TR6 might regulate T‐cell interaction with other cells such as antigen‐presenting cells (APC) or their fellow T cells by preventing them from forming inseparable cell clusters, which are undesirable for the progression of immune responses. © 2003 Wiley‐Liss, Inc.