CD4+ effector and memory cell populations protect against Cryptosporidium parvum infection

被引:13
|
作者
McNair, Nina N. [1 ,2 ]
Mead, Jan R. [1 ,2 ]
机构
[1] Atlanta VA Med Ctr, Decatur, GA 30033 USA
[2] Emory Univ, Dept Pediat, Atlanta, GA 30322 USA
基金
美国国家卫生研究院;
关键词
Cryptosporidium parvum; CD4(+) T cells; Memory; CD62L expression; IMMUNE-RESPONSES; ANTIGEN; SUSCEPTIBILITY; REINFECTION; CYTOKINE; IL-12;
D O I
10.1016/j.micinf.2013.04.009
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Cryptosporidium parvum is a protozoan parasite that infects the epithelial cells of the small intestine causing diarrheal illness in humans. While T cells are known to be important in resistance and recovery from infection, little has been characterized as to the phenotypic expression of surface effector and memory markers after infection. We used an acute model of infection (C57BL/6 interleukin-12p40), which develops long-standing resistance to re-infection, to characterize expression of different effector and memory cells. Using flow cytometry, we found that heterogeneous populations were generated after infection, consisting of both CD62L(high) central memory T cells (T-CM) and CD62L(low) effector memory T cells (T-EM) that were competent to produce the Th type 1 effector cytolcine, IFN-gamma. Both CD4(+) and CD8(+) T-CM and T-EM populations persisted in the absence of infection (up to 60 days post-infection). Additionally, transfer of either CD62L(low)CD4+ TEm or CD62(high)CD4+ T-CM into naive recipients resulted in a protective response. Taken together, these studies show that distinct subsets of effector and memory CD4+ T cells develop after infection with C. parvum, and mediate protective immunity to re-challenge. Published by Elsevier Masson SAS on behalf of Institut Pasteur.
引用
收藏
页码:599 / 606
页数:8
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