Montes de Oca Marcela, Engwerda Christian R, Kaye Paul M
York Biomedical Research Institute, Hull York Medical School, University of York, Heslington, York, United Kingdom.
QIMR Berghofer Medical Research Institute, Infectious Diseases Division, Brisbane, Queensland, Australia.
Cytokine X. 2020 Sep 1;2(4):100036. doi: 10.1016/j.cytox.2020.100036. eCollection 2020 Dec.
Visceral leishmaniasis (VL) causes extensive splenic pathology that contributes to dysfunctional immune responses, in part through displacement and destruction of cell populations involved in maintaining splenic structural integrity. The expression of pro and anti-inflammatory cytokines and chemokines is crucial in orchestrating the delicate balance that exists between host resistance and tissue pathology. In an effort to restore homeostatic balance to the local microenvironment, remodelling of the splenic architecture occurs in a compartmentalised manner to retain some level of functionality, despite persistent inflammatory pressures. Animal models of VL as well as human studies have significantly contributed to our understanding of the architectural changes that occur in the spleen during VL. Here, we review the role of cytokines in mediating microarchitectural changes associated with the development of splenomegaly during VL.
内脏利什曼病(VL)会导致广泛的脾脏病理变化,这在一定程度上会导致免疫反应功能失调,部分原因是参与维持脾脏结构完整性的细胞群体被取代和破坏。促炎和抗炎细胞因子及趋化因子的表达对于协调宿主抵抗力与组织病理之间存在的微妙平衡至关重要。为了恢复局部微环境的稳态平衡,尽管存在持续的炎症压力,但脾脏结构会以分区的方式进行重塑,以保留一定程度的功能。VL的动物模型以及人体研究极大地促进了我们对VL期间脾脏发生的结构变化的理解。在此,我们综述细胞因子在介导与VL期间脾肿大发展相关的微结构变化中的作用。