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T Cells are Unresponsive to Transgenic MHC Class II Molecules Expressed on Pancreatic β Cells
Author(s) -
Pilstro¨m B.,
Bo¨hme J.
Publication year - 1997
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 - 10.1046/j.1365-3083.1997.d01-410.x
Subject(s) - insulitis , mhc class ii , priming (agriculture) , cytotoxic t cell , biology , major histocompatibility complex , mhc class i , immunology , genetically modified mouse , microbiology and biotechnology , pancreatic islets , antigen presenting cell , antigen , t cell , mhc restriction , in vivo , transgene , in vitro , immune system , endocrinology , autoimmunity , insulin , islet , gene , genetics , botany , germination
It has been proposed that the autoimmune attack on the pancreatic β cells leading to insulin‐dependent diabetes mellitus can be caused by the expression of MHC class II molecules on the β cells. Transgenic mice expressing normal levels of allogeneic MHC class II A k on the β‐cell surface (IP‐A k ) do not develop either insulitis or diabetes, yet these mice are not tolerant to A k when expressed on normal antigen‐presenting cells. The authors have stimulated T cells from IP‐A k mice in vitro with A k ‐expressing β cells. Mice were also primed in vivo in order to facilitate the antiallogeneic response. The authors found that neither IP‐A k positive nor IP‐A k negative mice were able to respond to A k ‐expressing β cells, and that in vivo priming does not overcome this inability. They suggest that β cells do not act as antigen‐presenting cells, probably due to inability of delivering costimulatory signals. This strengthens the notion that MHC class II expression per se is not sufficient to induce an autoimmune attack on the β cells.