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Hydrocortisone Abrogates Proliferation of T Cells in Autologous Mixed Lymphocyte Reaction by Rendering the Interleukin‐2 Producer T Cells Unresponsive to Interleukin‐1 and Unable to Synthesize the T‐Cell Growth Factor
Author(s) -
PALACIOS R.,
SUGAWARA I.
Publication year - 1982
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1982.tb00618.x
Subject(s) - mixed lymphocyte reaction , interleukin 2 , interleukin , t lymphocyte , hydrocortisone , interleukin 4 , interleukin 3 , cytotoxic t cell , biology , microbiology and biotechnology , chemistry , t cell , immunology , endocrinology , cytokine , in vitro , biochemistry , immune system , interleukin 21
Hydrocortisone (HC‐A) inhibited the proliferative response in the autologous mixed lymphocyte reaction (AMLR). The inhibitory activity became apparent 48 h after initiation of the cultures and was maintained throughout the culture period. T cells from cultures treated with HC‐A showed a proliferative response to interleukin‐2 (IL‐2) of a similar degree as T cells from cultures not exposed to this drug. Hydrocortisone abrogated the production of IL‐2 in AMLR. The addition of interleukin‐1 (IL‐1) to HC‐A‐treated cultures did not restore or increase the synthesis of IL‐2, whereas IL‐1 added to non HC‐A‐treated cultures significantly enhanced the synthesis of IL‐2. Finally, IL‐2 but not IL‐1 could overcome the abrogatory effect of hydrocortisone on proliferation of T cells induced by AMLR. These results indicate that HC‐A inhibits proliferation of T cells in AMLR by causing the IL‐2 producer T cells to become unresponsive to IL‐1 and unable to synthesize IL‐2. This drug does not, however, interfere with the process by which resting T cells acquire responsiveness to IL‐2.