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- W4313385705 endingPage "208.15" @default.
- W4313385705 startingPage "208.15" @default.
- W4313385705 abstract "Abstract HIV causes a slowly progressive immunodeficiency disease via depletion of helper T cells and other immune cells, eventually resulting in AIDS. Currently, no effective vaccine exists for HIV. Acute HIV infection is associated with viral replication in, and of destruction of gut tissues. A key subset of gut-homing immune cells, CD4+ T cells expressing the integrin receptor α4β7, are highly susceptible to HIV infection. α4β7+/CD4+T cells gain entry to gut tissues by binding to MAdCAM, a receptor that is expressed on the surface of endothelial cells that line gut-associated lymphoid tissues (GALT). In a recent study of rhesus macaques infected with SIV we observed dramatic increases in levels of soluble MAdCAM in the serum shortly after infection. The presence of soluble MAdCAM in serum, correlated with viral replication in GALT, and suggested that MAdCAM was shed from the surface of endothelial cells in response to immune activation and inflammation of gut tissues. To investigate the regulation and functionality of MAdCAM, we generated distinct recombinant Rhesus macaque MAdCAM proteins including both soluble and membrane bound forms. Plate bound assays demonstrated that soluble rhesus MAdCAM can function as a T cell co-stimulatory signal. Human CD4+ T cells substantially proliferated in the presence of soluble rhesus MAdCAM proteins and proliferation diminished in the presence of the anti-α4β7 (ACT1) antibody. Importantly, since HIV infects GALT, which contains the majority of immune cells, the study of MAdCAM-α4β7 signaling and mechanisms of MAdCAM shedding may provide insight on potential mucosal-based therapies for treating HIV and serve as a biomarker of HIV-induced gut inflammation, respectively." @default.
- W4313385705 created "2023-01-06" @default.
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- W4313385705 date "2016-05-01" @default.
- W4313385705 modified "2023-09-23" @default.
- W4313385705 title "MAdCAM as a potential biomarker of HIV-induced inflammation" @default.
- W4313385705 doi "https://doi.org/10.4049/jimmunol.196.supp.208.15" @default.
- W4313385705 hasPublicationYear "2016" @default.
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