Bose Moumita, Jefferies Caroline
Division of Rheumatology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Research Division of Immunology, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Immunometabolism (Cobham). 2022 Jul 29;4(3):e00004. doi: 10.1097/IN9.0000000000000004. eCollection 2022 Jul.
Acknowledging sex differences in immune response is particularly important when we consider the differences between men and women in the incidence of disease. For example, over 80% of autoimmune disease occurs in women, whereas men have a higher incidence of solid tumors compared to women. In general women have stronger innate and adaptive immune responses than men, explaining their ability to clear viral and bacterial infections faster, but also contributing to their increased susceptibility to autoimmune disease. The autoimmune disease systemic lupus erythematosus (SLE) is the archetypical sexually dimorphic disease, with 90% of patients being women. Various mechanisms have been suggested to account for the female prevalence of SLE, including sex hormones, X-linked genes, and epigenetic regulation of gene expression. Here, we will discuss how these mechanisms contribute to pathobiology of SLE and how type I interferons work with them to augment sex specific disease pathogenesis in SLE.
当我们考虑男性和女性在疾病发病率上的差异时，认识到免疫反应中的性别差异尤为重要。例如，超过80%的自身免疫性疾病发生在女性身上，而与女性相比，男性实体瘤的发病率更高。一般来说，女性的先天免疫和适应性免疫反应比男性更强，这解释了她们能够更快清除病毒和细菌感染的能力，但也导致了她们对自身免疫性疾病易感性的增加。自身免疫性疾病系统性红斑狼疮（SLE）是典型的性别差异疾病，90%的患者为女性。已经提出了各种机制来解释SLE在女性中的患病率，包括性激素、X连锁基因和基因表达的表观遗传调控。在这里，我们将讨论这些机制如何促成SLE的病理生物学，以及I型干扰素如何与它们协同作用，增强SLE中性别特异性疾病的发病机制。
