Apoptosis in infectious diseases as a mechanism of immune evasion and survival

被引:25
|
作者
Quarleri, Jorge [1 ]
Cevallos, Cintia [1 ]
Delpino, Maria Victoria [2 ]
机构
[1] Univ Buenos Aires, CONICET, Inst Invest Biomed Retrovirus & Sida INBIRS, Buenos Aires, DF, Argentina
[2] Univ Buenos Aires, CONICET, Inst Inmunol Genet & Metab INIGEM, Buenos Aires, DF, Argentina
来源
关键词
TUMOR-NECROSIS-FACTOR; CELL-DEATH RECOMMENDATIONS; BCL-2 PROTEIN FAMILY; MYCOBACTERIUM-TUBERCULOSIS; NOMENCLATURE COMMITTEE; SIGNAL-TRANSDUCTION; PROSURVIVAL BCL-2; PROAPOPTOTIC BAX; KAPOSIS-SARCOMA; OUTER-MEMBRANE;
D O I
10.1016/bs.apcsb.2021.01.001
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In pluricellular organisms, apoptosis is indispensable for the development and homeostasis. During infection, apoptosis plays the main role in the elimination of infected cells. Infectious diseases control apoptosis, and this contributes to disease pathogenesis. Increased apoptosis may participate in two different ways. It can assist the dissemination of intracellular pathogens or induce immunosuppression to favor pathogen dissemination. In other conditions, apoptosis can benefit eradicate infectious agents from the host. Accordingly, bacteria, viruses, fungi, and parasites have developed strategies to inhibit host cell death by apoptosis to allow intracellular survival and persistence of the pathogen. The clarification of the intracellular signaling pathways, the receptors involved and the pathogen factors that interfere with apoptosis could disclose new therapeutic targets for blocking microbial actions on apoptotic pathways. In this review, we summarize the current knowledge on pathogen anti-apoptotic and apoptotic approaches and the mechanisms involving in disease.
引用
收藏
页码:1 / 24
页数:24
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