Published online Feb 12, 2015. doi: 10.5501/wjv.v4.i1.17
Peer-review started: August 6, 2014
First decision: September 16, 2014
Revised: September 30, 2014
Accepted: October 23, 2014
Article in press: October 27, 2014
Published online: February 12, 2015
Immunosenescence is marked by accelerated degradation of host immune responses leading to the onset of opportunistic infections, where senescent T cells show remarkably higher ontogenic defects as compared to healthy T cells. The mechanistic association between T-cell immunosenescence and human immunodeficiency virus (HIV) disease progression, and functional T-cell responses in HIV-tuberculosis (HIV-TB) co-infection remains to be elaborately discussed. Here, we discussed the association of immunosenescence and chronic immune activation in HIV-TB co-infection and reviewed the role played by mediators of immune deterioration in HIV-TB co-infection necessitating the importance of designing therapeutic strategies against HIV disease progression and pathogenesis.
Core tip: The mechanistic aspects associated with increased expression of senescence and immune activa-tion markers cluster of differentiation (CD) 38, CD69, CD57, human leukocyte antigen-DR, and the down-regulation of functional molecules, viz., CD28, CD27, CD40L and CD127 on human immunodeficiency virus-specific T cells appear to be crucial in the immunopathogenesis of HIV-tuberculosis (HIV-TB) co-infection. Mycobacterium tuberculosis appears to play a major role in accelerating HIV disease progression, by directly or indirectly facilitating factors associated with immune senescence. Measures to ameliorate immunosenescence and immune activation appear to stem from identification of novel targets of downstream senescence signaling. Restoration of molecules associated with T-cell homeostasis, differentiation, cell survival and proliferation abilities of HIV-specific CD8+ T cells is key to foster functional immune responses.