Effects of Low-Level Persistent Infection on Maintenance of Immunity by CD4 T Cell Subsets and Th1 Cytokines.
Effects of Low-Level Persistent Infection on Maintenance of Immunity by CD4 T Cell Subsets and Th1 Cytokines.
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DOI：
10.1128/iai.00531-22
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发表时间：
2023-03-15
影响因子：
3.1
通讯作者：
Stephens, Robin
中科院分区：
文献类型：
--
作者：
Ibitokou, Samad A. A.;Gbedande, Komi;Opata, Michael M. M.;Carpio, Victor H. H.;Marshall, Karis M. M.;Stephens, Robin
CD4 T cells are required, along with antibodies, for complete protection from blood-stage infection with Plasmodium spp., which cause malaria. Without continuous exposure, as on emigration of people from endemic areas, protection from malaria decays. As in other persistent infections, low-level Plasmodium chabaudi infection protects the host from reinfection at 2 months postinfection, a phenomenon termed premunition. Premunition is correlated with T cell responses, rather than antibody levels. We previously showed that while both effector T cells (Teff) and memory T cells (Tmem) are present after infection, Teff protect better than Tmem. Here, we studied T cell kinetics post-infection by labeling dividing Ifng+ T cells with 5-bromo-2′-deoxyuridine (BrdU) in infected Ifng reporter mice. Large drops in specific T cell numbers and Ifng+ cells upon clearance of parasites suggest a mechanism for decay of protection. Although protection decays, CD4 Tmem persist, including a highly differentiated CD27− effector memory (Tem) subset that maintains some Ifng expression. In addition, pretreatment of chronically infected animals with neutralizing antibody to interferon gamma (IFN-γ) or with clodronate liposomes before reinfection decreases premunition, supporting a role for Th1-type immunity to reinfection. A pulse-chase experiment comparing chronically infected to treated animals showed that recently divided Ifng+ T cells, particularly IFN-γ+ TNF+ IL-2− T cells, are promoted by persistent infection. These data suggest that low-level persistent infection reduces CD4+ Tmem and multifunctional Teff survival, but promotes IFN-γ+ TNF+ IL-2− T cells and Ifng+ terminally differentiated effector T cells, and prolongs immunity.
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影响因子：
4.1
作者：
Borges da Silva H;Fonseca R;Alvarez JM;D'Império Lima MR
通讯作者：
D'Império Lima MR
影响因子：
5.5
作者：
Ramesh Kumar J;Smith JP;Kwon H;Smith RC
通讯作者：
Smith RC
影响因子：
3.1
作者：
Li, C;Corraliza, I;Langhorne, J
通讯作者：
Langhorne, J
影响因子：
4.4
作者：
da Silva, Henrique Borges;de Salles, Erika Machado;D'Imperio Lima, Maria Regina
通讯作者：
D'Imperio Lima, Maria Regina
影响因子：
5.8
作者：
Carpio, Victor H.;Aussenac, Florentin;Stephens, Robin
通讯作者：
Stephens, Robin