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Mouse cytolytic T cells reactive with rat islet tumour RIN 5AH‐B cells
Author(s) -
SchØLler JØRGEN,
Rubin BENT
Publication year - 1990
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1699-0463.1990.tb01033.x
Subject(s) - cytotoxic t cell , major histocompatibility complex , antigen , biology , antigen presenting cell , epitope , t cell , cytolysis , microbiology and biotechnology , interleukin 21 , immunology , cd8 , immune system , in vitro , biochemistry
Insulin dependent (type 1) diabetes mellitus is considered to be an autoimmune disease characterized by a specific destruction of the insulin‐producing pancreatic β cells. We have explored the possibilities of raising T cells specific for putative pancreatic β‐cell autoantigens using a xenogeneic system. Mouse T cells were induced against the rat insulinoma cells RIN 5AH‐B (RIN) and tested for their specific reactivity. No MHC class II‐restricted β‐cell‐specific helper T‐cell reactivity could be detected within the bulk cultures as measured by proliferation, but a remarkably high cytotoxicity against the RIN cells was observed. The target antigen on the cell surface recognized by the generated cytotoxic T cells was shown to be the rat class I major histocompatibility antigen RT1 8 , and not a β‐cell or tumour cell‐specific antigen associated with RIN cell MHC molecules. Our results demonstrate that it is feasible to evoke a xenogeneic T‐cell response against the RIN cells. However, the mouse T cells recognize a dominant epitope present on the expressed rat class I major histocompatibility antigen RT1A 8 and not a β‐cell‐specific antigen. Hence, we conclude that it appears most unlikely that β‐cell‐specific T cells can be raised in the xenogeneic system.