Bowlus Christopher L
Department of Internal Medicine, University of California, Davis, 4635 2nd Avenue, Room 1004, Sacramento, CA 95817, USA.
Autoimmun Rev. 2003 Mar;2(2):73-8. doi: 10.1016/s1568-9972(02)00143-x.
Iron is a vital metal for the proliferation of all cells including those of the immune system. Iron deficiency causes several defects in both the humoral and cellular arms of immunity. One of the most profound changes is a reduction in peripheral T cells and atrophy of the thymus. The presence of transferrin receptor on immature, proliferating thymocytes and the inhibition of thymocyte proliferation and differentiation by anti-transferrin receptor antibody highlight the importance of iron to T cell development. Growing evidence suggests that T cells may in turn, regulate iron metabolism perhaps through interactions with the non-classical major histocompatibility complex gene HFE. The association of the iron transporter NRAMP1 with several autoimmune disorders along with evidence that iron can catalyze the production of cryptic epitopes of several autoantigens, establishes a potential role for iron in the development of autoimmunity.
铁是包括免疫系统细胞在内的所有细胞增殖所必需的金属。缺铁会导致体液免疫和细胞免疫的多项缺陷。最显著的变化之一是外周血T细胞减少和胸腺萎缩。未成熟的增殖性胸腺细胞上存在转铁蛋白受体，以及抗转铁蛋白受体抗体对胸腺细胞增殖和分化的抑制作用，突出了铁对T细胞发育的重要性。越来越多的证据表明，T细胞可能反过来调节铁代谢，或许是通过与非经典主要组织相容性复合体基因HFE相互作用来实现的。铁转运蛋白NRAMP1与多种自身免疫性疾病相关，同时有证据表明铁可催化几种自身抗原隐蔽表位的产生，这确立了铁在自身免疫性疾病发生发展中的潜在作用。
