Open AccessSuppression of HLA class II expression on thyrocytes by interferon‐alpha 1
Author(s) -
GUERIN V.,
TODD I.,
HAMMOND L. J.,
BOTTAZZO G. F.
Publication year - 1990
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.1365-2249.1990.tb08093.x
Subject(s) - human leukocyte antigen , immunology , interferon gamma , alpha (finance) , alpha interferon , in vitro , recombinant dna , lymphoblast , biology , interferon , cell culture , endocrinology , cytokine , medicine , antigen , gene , genetics , construct validity , nursing , patient satisfaction
SUMMARY Inappropriate expression of HLA class II molecules by human thyroid epithelial cells (thyrocytes) is commonly associated with autoimmune thyroid disease. HLA class 11 expression can be modulated in thyrocytes in vitro by a variety of substances: in particular, it is readily induced by interferon‐gamma (IFN‐γ). Here we show that recombinant IFN‐α1 (rIFN‐α1) does not induce HLA class II expression by thyrocytes. but rather it suppresses the induction of such expression by rIFN‐γ. Similar effects were observed with IFN‐α derived from a lymphoblastoid cell line. The effect of rIFN‐α1 on thyrocytes differs from its effect on human monocytes, reported by others, in which it was found to enhance the expression of HLA class II. Thus, rIFN‐α1 appears to have a differential effect on HLA class II expression, depending on the cell type involved.