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© Ahmed Haouz
Cristaux d'une protéine de Mycobacterium tuberculosis produits dans le cadre du Grand Programme Horizontal sur la Tuberculose à l'Institut Pasteur. La caractérisation structurale de protéines mycobactériennes aide à une meilleure compréhension de la physiologie et de la pathogénicité des mycobactéries et fournit un point de départ pour la conception de nouveaux agents antibactériens.
Publication : The Journal of clinical investigation

PLA2G1B is involved in CD4 anergy and CD4 lymphopenia in HIV-infected patients.

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in The Journal of clinical investigation - 01 Jun 2020

Pothlichet J, Rose T, Bugault F, Jeammet L, Meola A, Haouz A, Saul F, Geny D, Alcami J, Ruiz-Mateos E, Teyton L, Lambeau G, Thèze J,

Link to Pubmed [PMID] – 32436864

Link to DOI [DOI] – 10.1172/JCI131842131842

J. Clin. Invest. 2020 Jun; 130(6): 2872-2887

The precise mechanism leading to profound immunodeficiency of HIV-infected patients is still only partially understood. Here, we show that more than 80% of CD4+ T cells from HIV-infected patients have morphological abnormalities. Their membranes exhibited numerous large abnormal membrane microdomains (aMMDs), which trap and inactivate physiological receptors, such as that for IL-7. In patient plasma, we identified phospholipase A2 group IB (PLA2G1B) as the key molecule responsible for the formation of aMMDs. At physiological concentrations, PLA2G1B synergized with the HIV gp41 envelope protein, which appears to be a driver that targets PLA2G1B to the CD4+ T cell surface. The PLA2G1B/gp41 pair induced CD4+ T cell unresponsiveness (anergy). At high concentrations in vitro, PLA2G1B acted alone, independently of gp41, and inhibited the IL-2, IL-4, and IL-7 responses, as well as TCR-mediated activation and proliferation, of CD4+ T cells. PLA2G1B also decreased CD4+ T cell survival in vitro, likely playing a role in CD4 lymphopenia in conjunction with its induced IL-7 receptor defects. The effects on CD4+ T cell anergy could be blocked by a PLA2G1B-specific neutralizing mAb in vitro and in vivo. The PLA2G1B/gp41 pair constitutes what we believe is a new mechanism of immune dysfunction and a compelling target for boosting immune responses in HIV-infected patients.

https://pubmed.ncbi.nlm.nih.gov/32436864