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10.3389/fimmu.2017.01461

http://scihub22266oqcxt.onion/10.3389/fimmu.2017.01461
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C5673850!5673850!29163528
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suck abstract from ncbi


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pmid29163528      Front+Immunol 2017 ; 8 (ä): ä
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  • The Role of Transforming Growth Factor Beta-1 in the Progression of HIV/AIDS and Development of Non-AIDS-Defining Fibrotic Disorders #MMPMID29163528
  • Theron AJ; Anderson R; Rossouw TM; Steel HC
  • Front Immunol 2017[]; 8 (ä): ä PMID29163528show ga
  • Even after attainment of sustained viral suppression following implementation of highly active antiretroviral therapy, HIV-infected persons continue to experience persistent, low-grade, systemic inflammation. Among other mechanisms, this appears to result from ongoing microbial translocation from a damaged gastrointestinal tract. This HIV-related chronic inflammatory response is paralleled by counteracting, but only partially effective, biological anti-inflammatory processes. Paradoxically, however, this anti-inflammatory response not only exacerbates immunosuppression but also predisposes for development of non-AIDS-related, non-communicable disorders. With respect to the pathogenesis of both sustained immunosuppression and the increased frequency of non-AIDS-related disorders, the anti-inflammatory/profibrotic cytokine, transforming growth factor-?1 (TGF-?1), which remains persistently elevated in both untreated and virally suppressed HIV-infected persons, may provide a common link. In this context, the current review is focused on two different, albeit related, harmful activities of TGF-?1 in HIV infection. First, on the spectrum of anti-inflammatory/immunosuppressive activities of TGF-?1 and the involvement of this cytokine, derived predominantly from T regulatory cells, in driving disease progression in HIV-infected persons via both non-fibrotic and profibrotic mechanisms. Second, the possible involvement of sustained elevations in circulating and tissue TGF-?1 in the pathogenesis of non-AIDS-defining cardiovascular, hepatic, pulmonary and renal disorders, together with a brief comment on potential TGF-?1-targeted therapeutic strategies.
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