Molecular signatures of T-cell inhibition in HIV-1 infection

Cellular immune responses play a crucial role in the control of viral replication in HIV-infected individuals. However,the virus succeeds in exploiting the immune system to its advantage and therefore, the host ultimately fails to control the virus leading to development of terminal AIDS. The virus...

Full description

Bibliographic Details
Main Authors: Larsson, M., Shankar, E.M., Che, K.F., Saeldi, A., Ellegard, R., Barathan, M., Velu, V., Kamarulzaman, A.
Format: Article
Language:English
Published: BioMed Central 2013
Subjects:
Online Access:http://eprints.um.edu.my/9592/1/00000544_99598.pdf
_version_ 1796945946405240832
author Larsson, M.
Shankar, E.M.
Che, K.F.
Saeldi, A.
Ellegard, R.
Barathan, M.
Velu, V.
Kamarulzaman, A.
author_facet Larsson, M.
Shankar, E.M.
Che, K.F.
Saeldi, A.
Ellegard, R.
Barathan, M.
Velu, V.
Kamarulzaman, A.
author_sort Larsson, M.
collection UM
description Cellular immune responses play a crucial role in the control of viral replication in HIV-infected individuals. However,the virus succeeds in exploiting the immune system to its advantage and therefore, the host ultimately fails to control the virus leading to development of terminal AIDS. The virus adopts numerous evasion mechanisms to hijack the host immune system. We and others recently described the expression of inhibitory molecules on T cells as a contributing factor for suboptimal T-cell responses in HIV infection both in vitro and in vivo. The expression of these molecules that negatively impacts the normal functions of the host immune armory and the underlying signaling pathways associated with their enhanced expression need to be discussed. Targets to restrain the expression of these molecular markers of immune inhibition is likely to contribute to development of therapeutic interventions that augment the functionality of host immune cells leading to improved immune control of HIV infection. In this review, we focus on the functions of inhibitory molecules that are expressed or secreted following HIV infection such as BTLA, CTLA-4, CD160, IDO, KLRG1, LAG-3, LILRB1, PD-1, TRAIL, TIM-3, and regulatory cytokines, and highlight their significance in immune inhibition. We also highlight the ensemble of transcriptional factors such as BATF, BLIMP-1/PRDM1, FoxP3, DTX1 and molecular pathways that facilitate the recruitment and differentiation of suppressor T cells in response to HIV infection.
first_indexed 2024-03-06T05:24:14Z
format Article
id um.eprints-9592
institution Universiti Malaya
language English
last_indexed 2024-03-06T05:24:14Z
publishDate 2013
publisher BioMed Central
record_format dspace
spelling um.eprints-95922017-07-14T07:50:48Z http://eprints.um.edu.my/9592/ Molecular signatures of T-cell inhibition in HIV-1 infection Larsson, M. Shankar, E.M. Che, K.F. Saeldi, A. Ellegard, R. Barathan, M. Velu, V. Kamarulzaman, A. R Medicine Cellular immune responses play a crucial role in the control of viral replication in HIV-infected individuals. However,the virus succeeds in exploiting the immune system to its advantage and therefore, the host ultimately fails to control the virus leading to development of terminal AIDS. The virus adopts numerous evasion mechanisms to hijack the host immune system. We and others recently described the expression of inhibitory molecules on T cells as a contributing factor for suboptimal T-cell responses in HIV infection both in vitro and in vivo. The expression of these molecules that negatively impacts the normal functions of the host immune armory and the underlying signaling pathways associated with their enhanced expression need to be discussed. Targets to restrain the expression of these molecular markers of immune inhibition is likely to contribute to development of therapeutic interventions that augment the functionality of host immune cells leading to improved immune control of HIV infection. In this review, we focus on the functions of inhibitory molecules that are expressed or secreted following HIV infection such as BTLA, CTLA-4, CD160, IDO, KLRG1, LAG-3, LILRB1, PD-1, TRAIL, TIM-3, and regulatory cytokines, and highlight their significance in immune inhibition. We also highlight the ensemble of transcriptional factors such as BATF, BLIMP-1/PRDM1, FoxP3, DTX1 and molecular pathways that facilitate the recruitment and differentiation of suppressor T cells in response to HIV infection. BioMed Central 2013 Article PeerReviewed application/pdf en http://eprints.um.edu.my/9592/1/00000544_99598.pdf Larsson, M. and Shankar, E.M. and Che, K.F. and Saeldi, A. and Ellegard, R. and Barathan, M. and Velu, V. and Kamarulzaman, A. (2013) Molecular signatures of T-cell inhibition in HIV-1 infection. Retrovirology. pp. 1-14. ISSN 1742-4690, DOI https://doi.org/10.1186/1742-4690-10-31 <https://doi.org/10.1186/1742-4690-10-31>. doi:10.1186/1742-4690-10-31
spellingShingle R Medicine
Larsson, M.
Shankar, E.M.
Che, K.F.
Saeldi, A.
Ellegard, R.
Barathan, M.
Velu, V.
Kamarulzaman, A.
Molecular signatures of T-cell inhibition in HIV-1 infection
title Molecular signatures of T-cell inhibition in HIV-1 infection
title_full Molecular signatures of T-cell inhibition in HIV-1 infection
title_fullStr Molecular signatures of T-cell inhibition in HIV-1 infection
title_full_unstemmed Molecular signatures of T-cell inhibition in HIV-1 infection
title_short Molecular signatures of T-cell inhibition in HIV-1 infection
title_sort molecular signatures of t cell inhibition in hiv 1 infection
topic R Medicine
url http://eprints.um.edu.my/9592/1/00000544_99598.pdf
work_keys_str_mv AT larssonm molecularsignaturesoftcellinhibitioninhiv1infection
AT shankarem molecularsignaturesoftcellinhibitioninhiv1infection
AT chekf molecularsignaturesoftcellinhibitioninhiv1infection
AT saeldia molecularsignaturesoftcellinhibitioninhiv1infection
AT ellegardr molecularsignaturesoftcellinhibitioninhiv1infection
AT barathanm molecularsignaturesoftcellinhibitioninhiv1infection
AT veluv molecularsignaturesoftcellinhibitioninhiv1infection
AT kamarulzamana molecularsignaturesoftcellinhibitioninhiv1infection