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Transforming growth factor beta 1 (TGF‐β1) receptor expression on resting and mitogen‐activated T cells
Author(s) -
Ellingsworth Larry,
Nakayama Debra,
Dasch James,
Segarini Patricia,
Carrillo Pedro,
Waegell Wendy
Publication year - 1989
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.240390414
Subject(s) - autocrine signalling , transforming growth factor , concanavalin a , receptor , biology , microbiology and biotechnology , t cell , signal transduction , cell surface receptor , transforming growth factor beta , immunology , biochemistry , immune system , in vitro
Transforming growth factor β1 (TGF‐β1) is a potent autocrine growth inhibitor of lymphocytes. In this study, the expression of TGF‐β1 binding proteins was characterized on murine splenic T cells. With an affinity cross‐linking method and by neutralizing antibodies to TGF‐β1, [ 125 I] TGF‐β1 was found to bind to three cell surface–binding proteins (280–200 kD, 95–85 kD, 65 kD) that were differentially expressed on resting and mitogen‐stimulated T cells. Freshly prepared (resting) T cells were found to constitutively express the 95–85‐kD form of these binding proteins, whereas mitogenic stimulation by either concanavalin‐A (Con‐A), interleukin‐1 (IL‐1), interleukin‐2 (IL‐2), or 12‐tetradencanoyl‐phorbol‐13‐acetate (TPA) for 12–72 h induced the appearance of all forms of the TGF‐β1 binding proteins (280–200 kD, 95–85 kD, and 65 kD). Furthermore, antibodies that neutralized the biologic action of TGF‐β1 also blocked the binding of [ 125 I] TGF‐β1 to all three binding proteins, suggesting that these binding proteins are involved with signal transduction. These results suggest that the expression of the TGF‐β1 receptor on T cells is regulated by T cell mitogenic signals and that a regulatory relationship may exist between T cell growth‐promoting cytokines (IL‐1 and IL‐2) and the T cell growth inhibitor, TGF‐β1.