Pub Date : 2018-03-30DOI: 10.5772/INTECHOPEN.75169
M. Aguirre-Garcia, A. Escalona-Montaño, A. Wilkins-Rodríguez, L. Gutiérrez-Kobeh
Leishmania is the causative protozoan parasite of leishmaniasis. Distinct species provoke localized/diffuse cutaneous leishmaniasis or visceral leishmaniasis. Leishmania parasites have developed diverse strategies to evade the host immune response expressed through various cells, especially macrophages, NK cells, and dendritic cells. Participating in some of these strategies are Leishmania surface molecules, such as lipophosphoglycan (LPG) and protease gp63, which are thus considered virulence factors. LPG has been shown to modulate proinflammatory responses. For example, L. major LPG activates NK cells through tolllike receptor-2 (TLR2), while L. mexicana LPG elicits a differential production of cytokines in human dendritic cells and monocytes. Moreover, L. mexicana LPG activates MAP kinases in macrophages, which in turn enhance proinflammatory cytokine production through TLRs. Additionally, Leishmania exosomes have been found to strongly affect macrophage signaling and functions. Furthermore, proteins secreted by Leishmania promastigotes and amastigotes modulate the production of proinflammatory cytokines in human macrophages. Since Leishmania is an obligate intracellular parasite, its promastigotes utilize several mechanisms to survive and duplicate inside host cells, including the inhibition of apoptosis. It is now clear that MAPK p38, JNK, ERK 1/2, and PI3K/Akt participate in the inhibition of both natural and induced apoptosis of macrophages, neutrophils, and dendritic cells.
利什曼原虫是利什曼病的病原原生动物寄生虫。不同种类可引起局部/弥漫性皮肤利什曼病或内脏利什曼病。利什曼原虫寄生虫通过多种细胞，特别是巨噬细胞、NK细胞和树突状细胞，发展出多种逃避宿主免疫应答的策略。参与其中一些策略的是利什曼原虫表面分子，如脂磷酸聚糖(LPG)和蛋白酶gp63，因此它们被认为是毒力因子。液化石油气已被证明可以调节促炎反应。例如，L. major LPG通过toll样受体-2 (TLR2)激活NK细胞，而L. mexicana LPG在人树突状细胞和单核细胞中诱导细胞因子的差异产生。此外，L. mexicana LPG激活巨噬细胞中的MAP激酶，从而通过tlr增强促炎细胞因子的产生。此外，利什曼原虫外泌体已被发现强烈影响巨噬细胞的信号传导和功能。此外，利什曼原虫和无尾鞭毛原虫分泌的蛋白质调节人巨噬细胞中促炎细胞因子的产生。由于利什曼原虫是一种专性细胞内寄生虫，其原毛体利用多种机制在宿主细胞内存活和复制，包括抑制细胞凋亡。目前已经清楚，MAPK p38、JNK、ERK 1/2和PI3K/Akt参与抑制巨噬细胞、中性粒细胞和树突状细胞的自然和诱导凋亡。
{"title":"Immune Evasion Strategies","authors":"M. Aguirre-Garcia, A. Escalona-Montaño, A. Wilkins-Rodríguez, L. Gutiérrez-Kobeh","doi":"10.5772/INTECHOPEN.75169","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.75169","url":null,"abstract":"Leishmania is the causative protozoan parasite of leishmaniasis. Distinct species provoke localized/diffuse cutaneous leishmaniasis or visceral leishmaniasis. Leishmania parasites have developed diverse strategies to evade the host immune response expressed through various cells, especially macrophages, NK cells, and dendritic cells. Participating in some of these strategies are Leishmania surface molecules, such as lipophosphoglycan (LPG) and protease gp63, which are thus considered virulence factors. LPG has been shown to modulate proinflammatory responses. For example, L. major LPG activates NK cells through tolllike receptor-2 (TLR2), while L. mexicana LPG elicits a differential production of cytokines in human dendritic cells and monocytes. Moreover, L. mexicana LPG activates MAP kinases in macrophages, which in turn enhance proinflammatory cytokine production through TLRs. Additionally, Leishmania exosomes have been found to strongly affect macrophage signaling and functions. Furthermore, proteins secreted by Leishmania promastigotes and amastigotes modulate the production of proinflammatory cytokines in human macrophages. Since Leishmania is an obligate intracellular parasite, its promastigotes utilize several mechanisms to survive and duplicate inside host cells, including the inhibition of apoptosis. It is now clear that MAPK p38, JNK, ERK 1/2, and PI3K/Akt participate in the inhibition of both natural and induced apoptosis of macrophages, neutrophils, and dendritic cells.","PeriodicalId":17975,"journal":{"name":"Leishmaniases as Re-emerging Diseases","volume":"45 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73564945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：