Abstract
HLA class II molecules are surface glycoproteins which are essential in the initiation of immune responses. It has been postulated that induction of class II in epithelial cells such as endocrine cells, which are normally class II negative1, may result in autoimmunity2. In type I diabetes, islet beta cells, the target of the autoimmune process, selectively express class II antigens3,4. But in contrast to most other cell types5, islet beta cells are not stimulated to express class II by interferon-γ (IFN-γ)6,7 and thus the conditions under which this induction occurs have been particularly elusive. The cytotoxins tumour necrosis factor (TNF) and lymphotoxin (LT) synergize with IFN-γ in a number of activities8. We report here that IFN-γ in combination with either TNF or LT induces islet cell class II expression. This finding has important implications for the pathogenesis of type I diabetes and the understanding of the differential control of class II expression.
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Pujol–Borrell, R., Todd, I., Doshi, M. et al. HLA class II induction in human islet cells by interferon-γ plus tumour necrosis factor or lymphotoxin . Nature 326, 304–306 (1987). https://doi.org/10.1038/326304a0
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DOI: https://doi.org/10.1038/326304a0
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