Todd I, Pujol-Borrell R, Hammond L J, Bottazzo G F, Feldmann M
Clin Exp Immunol. 1985 Aug;61(2):265-73.
We recently showed that human thyroid epithelial cells, which are normally negative for HLA-DR molecules, express HLA-DR in thyroid autoimmunity. Furthermore, induction of HLA-DR on normal thyroid cells can be achieved by culture with plant lectins. We have now found that recombinant human interferon-gamma (IFN-gamma) induces expression of HLA-DR molecules on cultured human thyroid cells, whereas Namalva IFN-alpha, recombinant IFN-beta or recombinant interleukin-2 (IL-2) do not. All three IFN, but not IL-2, enhanced thyroid cell HLA-A,B,C expression. The results strongly implicate T cells (which are the source of IFN-gamma) in the aberrant induction of DR on thyroid epithelial cells which is proposed to be a central feature of the immunopathological processes leading to autoimmunity.
我们最近发现,正常情况下对HLA - DR分子呈阴性的人甲状腺上皮细胞,在甲状腺自身免疫中会表达HLA - DR。此外,通过与植物凝集素培养,可使正常甲状腺细胞诱导表达HLA - DR。我们现在发现,重组人干扰素 - γ(IFN - γ)可诱导培养的人甲状腺细胞表达HLA - DR分子,而Namalva干扰素 - α、重组干扰素 - β或重组白细胞介素 - 2(IL - 2)则不能。所有这三种干扰素,但不是IL - 2,可增强甲状腺细胞HLA - A、B、C的表达。这些结果有力地表明,T细胞(IFN - γ的来源)在甲状腺上皮细胞上DR的异常诱导中起作用,而这种异常诱导被认为是导致自身免疫的免疫病理过程的核心特征。