Role of TGF-beta and PGE2 in T cell responses during Plasmodium yoelii infection.
Role of TGF-beta and PGE2 in T cell responses during Plasmodium yoelii infection.
复制标题
约氏疟原虫感染期间 TGF-β 和 PGE2 在 T 细胞反应中的作用。
DOI：
10.1002/eji.200737068
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发表时间：
2007
影响因子：
5.4
通讯作者：
Rodriguez,Ana
中科院分区：
文献类型：
--
作者：
Ocaña-Morgner,Carlos;Wong,KurtA;Lega,Flavia;Dotor,Javier;Borras-Cuesta,Francisco;Rodriguez,Ana
During an acute blood‐stage malaria infection, T cell responses to malaria and other bystander antigens are inhibited.Plasmodiuminfection induces strong cytokine responses that facilitate parasite clearance but may interfere with T cell functions, as some of the soluble immune mediators induced are also general inhibitors of T cell responses. Using a malaria mouse model, we have analyzed the cytokines produced by dendritic cells in response toP. yoeliiinfection that have potential T cell inhibitory activity. We found that during acute infection DC migrate to the spleen and secrete TGF‐β, prostaglandin E2(PGE2) and IL‐10. We have analyzed the role of these general T cell inhibitors in a particular T cell response of evident importance in malaria infections: the CD8+T cells generated against the liver‐stage of the disease. During blood‐stage infection, inhibition of the activity of TGF‐β and PGE2restores the CD8+T cell responses generated by sporozoites, increasing protection against re‐infection. Our findings suggest that the strong cytokine response induced by blood‐stageP. yoeliiinfection affects host T cell responses, inhibiting protective CD8+T cells against the liver‐stage of the disease.
