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- W2938492236 abstract "Multiple obligatory intracellular bacteria in the genus Chlamydia are important pathogens. In humans, strains of C. trachomatis cause trachoma, chlamydia, and lymphogranuloma venereum. These diseases are all associated with extended courses of infection and reinfection that likely reflect the ability of chlamydiae to evade various aspects of host immune responses. Interferon-stimulated genes, driven in part by the cytokine interferon gamma, restrict the host range of various Chlamydia species, but how these pathogens evade interferon-stimulated genes in their definitive host is poorly understood. Various Chlamydia species can inhibit death of their host cells and may have evolved this strategy to evade prodeath signals elicited by host immune responses. We present evidence that chlamydia-induced programmed cell death resistance evolved to counter interferon- and immune-mediated killing of Chlamydia -infected cells." @default.
- W2938492236 created "2019-04-25" @default.
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- W2938492236 date "2019-04-30" @default.
- W2938492236 modified "2023-10-14" @default.
- W2938492236 title "Genetic Screen in Chlamydia muridarum Reveals Role for an Interferon-Induced Host Cell Death Program in Antimicrobial Inclusion Rupture" @default.
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- W2938492236 doi "https://doi.org/10.1128/mbio.00385-19" @default.
- W2938492236 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6456753" @default.
- W2938492236 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30967464" @default.
- W2938492236 hasPublicationYear "2019" @default.
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