dc.contributor.author |
Theron, Annette J.
|
|
dc.contributor.author |
Anderson, Ronald
|
|
dc.contributor.author |
Rossouw, Theresa M.
|
|
dc.contributor.author |
Steel, Helen C.
|
|
dc.date.accessioned |
2017-11-30T07:23:27Z |
|
dc.date.available |
2017-11-30T07:23:27Z |
|
dc.date.issued |
2017-11-02 |
|
dc.description.abstract |
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 HIVrelated
chronic inflammatory response is paralleled by counteracting, but only partially
effective, biological anti-inflammatory processes. Paradoxically, however, this antiinflammatory
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-β1 (TGF-β1), 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-β1 in
HIV infection. First, on the spectrum of anti-inflammatory/immunosuppressive activities
of TGF-β1 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-β1 in the pathogenesis of non-AIDS-defining cardiovascular,
hepatic, pulmonary and renal disorders, together with a brief comment on potential
TGF-β1-targeted therapeutic strategies. |
en_ZA |
dc.description.department |
Immunology |
en_ZA |
dc.description.librarian |
am2017 |
en_ZA |
dc.description.uri |
http://www.frontiersin.org/Immunology |
en_ZA |
dc.identifier.citation |
Theron AJ, Anderson R,
Rossouw TM and Steel HC (2017)
The Role of Transforming Growth
Factor Beta-1 in the Progression of
HIV/AIDS and Development of
Non-AIDS-Defining
Fibrotic Disorders.
Front. Immunol. 8:1461.
DOI: 10.3389/fimmu.2017.01461. |
en_ZA |
dc.identifier.issn |
1664-3224 (online) |
|
dc.identifier.other |
10.3389/fimmu.2017.01461 |
|
dc.identifier.uri |
http://hdl.handle.net/2263/63388 |
|
dc.language.iso |
en |
en_ZA |
dc.publisher |
Frontiers Research Foundation |
en_ZA |
dc.rights |
© 2017 Authors.
This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). |
en_ZA |
dc.subject |
Highly active antiretroviral therapy |
en_ZA |
dc.subject |
Immunosuppression |
en_ZA |
dc.subject |
Lymphoid fibrosis |
en_ZA |
dc.subject |
Macrophages |
en_ZA |
dc.subject |
Non-AIDSdefining defining disorders |
en_ZA |
dc.subject |
Non-AIDS defining disorders |
en_ZA |
dc.subject |
Organ fibrosis |
en_ZA |
dc.subject |
T Regulatory cells |
en_ZA |
dc.subject |
Antiretroviral therapy (ART) |
en_ZA |
dc.subject |
Myocardial infarction |
en_ZA |
dc.subject |
Microbial translocation |
en_ZA |
dc.subject |
Transforming growth factor-β1 (TGF-β1) |
en_ZA |
dc.subject |
Obstructive pulmonary disease |
en_ZA |
dc.subject |
Hepatitis-C virus |
en_ZA |
dc.subject |
Chronic kidney disease |
en_ZA |
dc.subject |
HIV infected patients |
en_ZA |
dc.subject |
Human immunodeficiency virus (HIV) |
en_ZA |
dc.subject |
Regulatory T-cells |
en_ZA |
dc.title |
The role of transforming growth factor beta-1 in the progression of HIV/AIDS and development of non-AIDS-defining fibrotic disorders |
en_ZA |
dc.type |
Article |
en_ZA |