Department of Immunobiology and Howard Hughes Medical Institute, Yale University School of Medicine, 300, Cedar Street, New Haven, CT 06520-8011, USA.
Curr Opin Immunol. 2013 Feb;25(1):103-8. doi: 10.1016/j.coi.2012.11.006. Epub 2012 Dec 12.
Gamma-interferon-inducible lysosomal thiol reductase (GILT), a thioredoxin-related oxidoreductase, functions in MHC class II-restricted antigen processing and MHC class I-restricted cross-presentation by reducing disulfide bonds of endocytosed proteins and facilitating their unfolding and optimal degradation. However, recent reports have greatly expanded our understanding of GILT's function. Several studies of GILT and antigen processing have shown that the influence of GILT on the peptide repertoire can alter the character of the immune response and affect central tolerance. Furthermore, a few unexpected roles for GILT have been uncovered: as a host factor for Listeria monocytogenes infection, in the maintenance of cellular glutathione (GSH) levels, and possibly outside the cell, as enzymatically active GILT is secreted by activated macrophages.
γ-干扰素诱导的溶酶体硫醇还原酶(GILT)是一种与硫氧还蛋白相关的氧化还原酶,它通过还原内吞蛋白的二硫键并促进其展开和最佳降解,从而参与 MHC Ⅱ类限制的抗原加工和 MHC Ⅰ类限制的交叉呈递。然而,最近的研究大大扩展了我们对 GILT 功能的理解。几项关于 GILT 和抗原加工的研究表明,GILT 对肽库的影响可以改变免疫反应的特征并影响中枢耐受。此外,还发现了 GILT 的一些意外作用:作为李斯特菌感染的宿主因子,在维持细胞谷胱甘肽(GSH)水平中,以及可能在细胞外,因为激活的巨噬细胞分泌具有酶活性的 GILT。