Martinelli Serena, Nannini Giulia, Cianchi Fabio, Coratti Francesco, Amedei Amedeo
Department of Clinical and Experimental Medicine, University of Florence, 50139 Florence, Italy.
SOD of Interdisciplinary Internal Medicine, Azienda Ospedaliera Universitaria Careggi (AOUC), 50134 Florence, Italy.
Biomedicines. 2024 Mar 8;12(3):616. doi: 10.3390/biomedicines12030616.
Autoimmune diseases are complex multifactorial disorders, and a mixture of genetic and environmental factors play a role in their onset. In recent years, the microbiota has gained attention as it helps to maintain host health and immune homeostasis and is a relevant player in the interaction between our body and the outside world. Alterations (dysbiosis) in its composition or function have been linked to different pathologies, including autoimmune diseases. Among the different microbiota functions, there is the activation/modulation of immune cells that can protect against infections. However, if dysbiosis occurs, it can compromise the host's ability to protect against pathogens, contributing to the development and progression of autoimmune diseases. In some cases, infections can trigger autoimmune diseases by several mechanisms, including the alteration of gut permeability and the activation of innate immune cells to produce pro-inflammatory cytokines that recruit autoreactive T and B cells. In this complex scenario, we cannot neglect critical hormones' roles in regulating immune responses. Different hormones, especially estrogens, have been shown to influence the development and progression of autoimmune diseases by modulating the activity and function of the immune system in different ways. In this review, we summarized the main mechanisms of connection between infections, microbiota, immunity, and hormones in autoimmune diseases' onset and progression given the influence of some infections and hormone levels on their pathogenesis. In detail, we focused on rheumatoid arthritis, multiple sclerosis, and systemic lupus erythematosus.
自身免疫性疾病是复杂的多因素疾病,遗传和环境因素的混合作用在其发病过程中发挥作用。近年来,微生物群受到关注,因为它有助于维持宿主健康和免疫稳态,并且在我们身体与外部世界的相互作用中扮演重要角色。其组成或功能的改变(生态失调)与包括自身免疫性疾病在内的不同病理状况有关。在微生物群的不同功能中,有免疫细胞的激活/调节,这可以预防感染。然而,如果发生生态失调,它会损害宿主抵御病原体的能力,从而导致自身免疫性疾病的发生和发展。在某些情况下,感染可通过多种机制引发自身免疫性疾病,包括肠道通透性的改变以及先天免疫细胞的激活,从而产生促炎细胞因子,进而招募自身反应性T细胞和B细胞。在这种复杂的情况下,我们不能忽视关键激素在调节免疫反应中的作用。不同的激素,尤其是雌激素,已被证明通过以不同方式调节免疫系统的活性和功能来影响自身免疫性疾病的发生和发展。在这篇综述中,鉴于一些感染和激素水平对自身免疫性疾病发病机制的影响,我们总结了感染、微生物群、免疫和激素在自身免疫性疾病发生和发展过程中的主要联系机制。详细地说,我们重点关注类风湿性关节炎、多发性硬化症和系统性红斑狼疮。