Laboratory of Molecular Immunopathology, Department of Clinical Pathology, Federal University of Paraná, Curitiba, Brazil.
Department of Pathology, Division of Immunology, School of Medicine, Johns Hopkins University, Baltimore, MD, United States.
Front Immunol. 2018 Aug 6;9:1842. doi: 10.3389/fimmu.2018.01842. eCollection 2018.
Chagas disease (CD), a neglected tropical disease caused by the protozoan , affects around six million individuals in Latin America. Currently, CD occurs worldwide, becoming a significant public health concern due to its silent aspect and high morbimortality rate. presents different escape strategies which allow its evasion from the host immune system, enabling its persistence and the establishment of chronic infection which leads to the development of chronic Chagas cardiomyopathy (CCC). The potent immune stimuli generated by persistence may result in tissue damage and inflammatory response. In addition, molecular mimicry between parasites molecules and host proteins may result in cross-reaction with self-molecules and consequently in autoimmune features including autoantibodies and autoreactive cells. Although controversial, there is evidence demonstrating a role for autoimmunity in the clinical progression of CCC. Nevertheless, the exact mechanism underlying the generation of an autoimmune response in human CD progression is unknown. In this review, we summarize the recent findings and hypotheses related to the autoimmune mechanisms involved in the development and progression of CCC.
恰加斯病(CD)是一种由原生动物引起的被忽视的热带病,影响拉丁美洲约六百万个人。目前,CD 发生在全球范围内,由于其隐匿性和高病死率,成为一个重大的公共卫生关注问题。 表现出不同的逃逸策略,使其能够逃避宿主免疫系统,从而使其持续存在并导致慢性感染,进而发展为慢性恰加斯心肌病(CCC)。 持续存在产生的强烈免疫刺激可能导致组织损伤和炎症反应。此外,寄生虫分子与宿主蛋白之间的分子模拟可能导致与自身分子的交叉反应,从而导致包括自身抗体和自身反应性细胞在内的自身免疫特征。尽管存在争议,但有证据表明自身免疫在 CCC 的临床进展中起作用。然而,在人类 CD 进展中产生自身免疫反应的确切机制尚不清楚。在这篇综述中,我们总结了与参与 CCC 发展和进展的自身免疫机制相关的最新发现和假设。