Open AccessInteraction of IL‐1β, IL‐6 and tumour necrosis factor‐alpha (TNF‐α) in human T cells activated by murine antigens
Author(s) -
PANZER S.,
MADDEN M.,
MATSUKI K.
Publication year - 1993
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1993.tb08203.x
Subject(s) - tumor necrosis factor alpha , cytokine , biology , beta (programming language) , antigen , cd8 , t cell , immunology , microbiology and biotechnology , immune system , computer science , programming language
SUMMARY We used a mixed leucocyte culture between human T cells and irradiated murine splenocytes which allowed us to distinguish between cytokine production from the responder and stimulator cells by the use of species‐specific assays for mRNA up‐regulation. Using this model of T cell activation by antigen, we studied the effects of human antigen‐presenting cell‐derived cytokines IL‐1β, IL‐6 and TNF‐α on the activation of human T cell subsets. We show in this system that exogenously added IL‐1β, IL‐6 and TNF‐α induces IL‐2 receptor (R) up‐regulation and IL‐2 production, and proliferation by both CD4 + and CD8 + cells. The addition of IL‐1β induces IL‐6 mRNA, and anti‐IL‐1 antibodies or an IL‐1R antagonist protein completely suppresses IL‐6 and TNF‐α supported proliferation. Similarily, addition of IL‐6 or TNF‐α induces up‐regulation of IL‐1β mRNA. However, anti‐IL‐6 and anti‐IL‐6R antibodies only partially block proliferation supported by IL‐1β. These findings suggest that IL‐6 and TNF‐α will induce IL‐2R up‐regulation/IL‐2 secretion via the induction of IL‐β production.