Year-end Sale % OFF 
Abstract
In our work, we analyzed the role of the CD100/CD72 and PD-1/PD-L1 axes in immune response dysfunction in human immunodeficiency virus (HIV)-1 infection in which high expressions of PD-1 and PD-L1 were associated with an immunosuppressive state via limitation of the HIV-1-specific T-cell responses. CD100 was demonstrated to play a relevant role in immune responses in various pathological processes and may be responsible for immune dysregulation during HIV-1 infection. We investigated the function of CD72/CD100, and PD-1/PDL-1 axes on T and B cells in HIV-infected individuals and in healthy individuals. We analyzed the frequencies and fluorescence intensities of these four markers on CD4+, CD8+ T and B cells. Marker expressions were increased during active HIV-1 infection. CD100 frequency on T cells was positively associated with the expression of PD-1 and PD-L1 on T cells from HIV-infected treatment-naïve individuals. In addition, the frequency of CD72-expressing T cells was associated with interferon gamma (IFN-γ) production in HIV-infected treatment-naïve individuals. Our data suggest that the CD72/CD100 and PD-1/PD-L1 axes may jointly participate in dysregulation of immunity during HIV-1 infection and could partially explain the immune systems’ hyper-activation and exhaustion.
Highlights
Dysregulation of human immunodeficiency virus (HIV)-specific T and B-cell responses is the principal cause for the lack of control of HIV replication
We evaluated 39 individuals divided into three groups: (i) Thirteen viral load (VL) individuals, HIV+ individuals that did not receive antiretroviral treatment and presented with detectable VL in
Efficient antiretroviral treatment permitted a reversion of such high expression, except for the levels of CD72 expression at CD4+ and CD8+ T cell surfaces
Summary
Dysregulation of HIV-specific T and B-cell responses is the principal cause for the lack of control of HIV replication. Chronic infection with the persistent presence of viral antigens gives rise to B- and T-cell exhaustion, which is characterized by loss of proliferative capacity and effector functions [1, 2]. Negative regulatory pathways (such as the PD-1/PD-L1 axis) under. CD72/CD100 and PD-1/PD-L1 axes in HIV-1+ individuals.
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
