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HIV-1 Infection Results in Sphingosine-1-Phosphate Receptor 1 Dysregulation in the Human Thymus. | LitMetric

AI Article Synopsis

  • - The study explores how HIV-1 infection impacts the regeneration of functional naïve T lymphocytes in individuals living with HIV, particularly focusing on the signaling pathway involved in their egress from the thymus.
  • - Researchers found that HIV-1 infection leads to an increased expression of Sphingosine-1-phosphate receptor 1 (S1PR1) in human thymus tissue, which is influenced by inflammatory cytokines like Interferon-Beta and Tumor Necrosis Factor-Alpha.
  • - The findings indicate that the enhanced expression of S1PR1 during HIV infection may cause immature thymocytes to exit the thymus prematurely, potentially compromising the immune function of those living with HIV.

Article Abstract

Regeneration of functional naïve T lymphocytes following the onset of human immunodeficiency virus (HIV) infection remains a crucial issue for people living with HIV (PLWH), even when adhering to antiretroviral therapy (ART). Thus far, reports on the impact of HIV-1 infection on the entry of thymic precursors and the egress of functional naïve T lymphocytes to and from the thymus are limited. We examined the impact of HIV-1 on Sphingosine-1-phosphate (S1P) signaling, which governs the egress of functional naïve thymocytes from the thymus to the periphery. Using in vitro experiments with primary human thymocytes and in vivo and ex vivo studies with humanized mice, we show that HIV-1 infection results in upregulation of the expression of S1P receptor 1 (S1PR1) in the human thymus. Intriguingly, this upregulation occurs during intrathymic infection (direct infection of the human thymic implant) as well as systemic infection in humanized mice. Moreover, considering the dysregulation of pro- and anti-inflammatory cytokines in infected thymi, the increased expression of S1PR1 in response to in vitro exposure to Interferon-Beta (IFN-β) and Tumor Necrosis Factor-Alpha (TNF-α) indicates that cytokine dysregulation following HIV infection may contribute to upregulation of S1PR1. Finally, an increased presence of CD3hiCD69- (fully mature) as well as CD3hiCD69+ (less mature) T cells in the spleen during HIV infection in humanized mice, combined with earlier expression of S1PR1 during thymocyte development, suggests that upregulation of S1PR1 may translate to increased or accelerated egress from the thymus. The egress of thymocytes that are not functionally mature from the thymus to peripheral blood and lymphoid organs may have implications for the immune function of PLWH.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10531245PMC
http://dx.doi.org/10.3390/ijms241813865DOI Listing

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