Romani L
Microbiology Section, Department of Experimental Medicine and Biochemical Sciences, University of Perugia, Italy.
Curr Opin Microbiol. 1999 Aug;2(4):363-7. doi: 10.1016/S1369-5274(99)80064-2.
Resistance to Candida albicans infection in mice results from the development of T helper (Th) type 1 cell responses. Cytokines produced by Th1 cells activate macrophages and neutrophils to a candidacidal state. The development of Th2 responses underlines susceptibility to infection, because cytokines produced by Th2 cells inhibit Th1 development and deactivate phagocytic effector cells. With the recognition of the reciprocal influences between innate and adaptive Th immunity, it appears that the coordinated action of these two lines of immune defense is required to efficiently oppose the infectivity of the fungus and to determine its lifelong commensalism at the mucosal level.
小鼠对白念珠菌感染的抵抗力源于1型辅助性T（Th1）细胞应答的发展。Th1细胞产生的细胞因子可将巨噬细胞和中性粒细胞激活至杀念珠菌状态。Th2应答的发展表明易感性增加，因为Th2细胞产生的细胞因子会抑制Th1的发展并使吞噬效应细胞失活。随着对天然免疫和适应性Th免疫之间相互影响的认识，似乎需要这两种免疫防御途径的协同作用，才能有效对抗真菌的感染性，并在黏膜水平决定其终生共生状态。
