Generalized immune activation as a direct result of activated CD4+T cell killing View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2009-10

AUTHORS

Rute Marques, Adam Williams, Urszula Eksmond, Andy Wullaert, Nigel Killeen, Manolis Pasparakis, Dimitris Kioussis, George Kassiotis

ABSTRACT

BACKGROUND: In addition to progressive CD4(+) T cell immune deficiency, HIV infection is characterized by generalized immune activation, thought to arise from increased microbial exposure resulting from diminishing immunity. RESULTS: Here we report that, in a virus-free mouse model, conditional ablation of activated CD4(+) T cells, the targets of immunodeficiency viruses, accelerates their turnover and produces CD4(+) T cell immune deficiency. More importantly, activated CD4(+) T cell killing also results in generalized immune activation, which is attributable to regulatory CD4(+) T cell insufficiency and preventable by regulatory CD4(+) T cell reconstitution. Immune activation in this model develops independently of microbial exposure. Furthermore, microbial translocation in mice with conditional disruption of intestinal epithelial integrity affects myeloid but not T cell homeostasis. CONCLUSIONS: Although neither ablation of activated CD4(+) T cells nor disruption of intestinal epithelial integrity in mice fully reproduces every aspect of HIV-associated immune dysfunction in humans, ablation of activated CD4(+) T cells, but not disruption of intestinal epithelial integrity, approximates the two key immune alterations in HIV infection: CD4(+) T cell immune deficiency and generalized immune activation. We therefore propose activated CD4(+) T cell killing as a common etiology for both immune deficiency and activation in HIV infection. More... »

PAGES

93

References to SciGraph publications

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1186/jbiol194

    DOI

    http://dx.doi.org/10.1186/jbiol194

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1025505792

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/19943952


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