Frontiers in immunology · 2026
Phenotypic characterization of mucosal-associated invariant T cells in visceral leishmaniasis and HIV co-infection.
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Pereira Victoria Hellena Silva, Nogueira Gustavo Augusto Fonseca, Borges-Fernandes Luana, de Carvalho Silvia Hees, Nogueira Adelina Machado de Carvalho, Araújo Argus Leão, Brito-de-Sousa Joaquim Pedro, Rodrigues Juliana Assunção, Toledo João Paulo Resende Magalhães, Magalhães Vanessa Caroline Randi, de Carvalho Jairo Campos, da Cunha Livia Fulgencio, Coelho-Dos-Reis Jordana Grazziela Alves, Teixeira-Carvalho Andréa, Martins-Filho Olindo Assis, Guimarães Gabriel Macedo Costa, Peruhype-Magalhães Vanessa
Аннотация
INTRODUCTION: Mucosal-associated invariant T (MAIT) cells are unconventional T lymphocytes with innate-like antimicrobial responsiveness. Despite their recognized role in bacterial and viral infections, their involvement in protozoal diseases, particularly visceral leishmaniasis (VL) and HIV co-infection, remains poorly understood.
METHODS: A cross-sectional study evaluated the immunophenotypic profile of circulating MAIT cells in visceral leishmaniasis patients (VL, n = 8), VL-HIV co-infection patients (VL-HIV, n = 10), VL-HIV coinfected patients under liposomal amphotericin B prophylactic treatment (VL-HIV(T), n = 9), and reference groups comprising HIV-mono-infected (HIV, n = 11) and non-infected (NI, n = 11) individuals. Multiparameter flow cytometry assessed MAIT cell frequency, subset distribution (CD4+, CD8+ and CD4-CD8-), and the expression of activation, costimulatory, cytotoxic, exhaustion and memory markers. Integrative correlation network analysis was performed to evaluate immunological interactions among MAIT cell markers.
RESULTS: MAIT cell frequencies were significantly reduced in VL and VL-HIV, predominantly affecting the CD8+ subset. Fold-change analyses demonstrated increased activation and cytotoxicity signatures in VL and VL-HIV patients, with marked upregulation of CD69, CD38, NKG2D, and CD107A, concomitant with increased expression of inhibitory receptors (PD-1, TIM-3, LAG-3), particularly in CD8+ and CD4-CD8- MAIT cells. In contrast, VL-HIV(T) patients exhibited a decrease in this hyperactivated/exhausted phenotype and partial restoration of central memory-associated features, suggesting immune rebalancing under treatment. Integrative correlation network analysis revealed marked differences of MAIT cell immunological interactions. VL and VL-HIV groups displayed reduced network density, decreased selective axis connectivity, and fragmentation of interactions among activation, cytotoxicity, and memory nodes, consistent with immune disorganization. Conversely, treated VL-HIV(T) patients exhibited increased connectivity and re-establishment of coordinated interactions between functional markers, indicating partial re-establishment of the MAIT cell immunological network architecture.
DISCUSSION: Together, VL and VL-HIV co-infection are associated with quantitative depletion and qualitative dysregulation of circulating MAIT cells, characterized by concurrent hyperactivation and exhaustion, coupled with immunological network fragmentation, while liposomal amphotericin B treatment appears to promote partial immunological reorganization.
METHODS: A cross-sectional study evaluated the immunophenotypic profile of circulating MAIT cells in visceral leishmaniasis patients (VL, n = 8), VL-HIV co-infection patients (VL-HIV, n = 10), VL-HIV coinfected patients under liposomal amphotericin B prophylactic treatment (VL-HIV(T), n = 9), and reference groups comprising HIV-mono-infected (HIV, n = 11) and non-infected (NI, n = 11) individuals. Multiparameter flow cytometry assessed MAIT cell frequency, subset distribution (CD4+, CD8+ and CD4-CD8-), and the expression of activation, costimulatory, cytotoxic, exhaustion and memory markers. Integrative correlation network analysis was performed to evaluate immunological interactions among MAIT cell markers.
RESULTS: MAIT cell frequencies were significantly reduced in VL and VL-HIV, predominantly affecting the CD8+ subset. Fold-change analyses demonstrated increased activation and cytotoxicity signatures in VL and VL-HIV patients, with marked upregulation of CD69, CD38, NKG2D, and CD107A, concomitant with increased expression of inhibitory receptors (PD-1, TIM-3, LAG-3), particularly in CD8+ and CD4-CD8- MAIT cells. In contrast, VL-HIV(T) patients exhibited a decrease in this hyperactivated/exhausted phenotype and partial restoration of central memory-associated features, suggesting immune rebalancing under treatment. Integrative correlation network analysis revealed marked differences of MAIT cell immunological interactions. VL and VL-HIV groups displayed reduced network density, decreased selective axis connectivity, and fragmentation of interactions among activation, cytotoxicity, and memory nodes, consistent with immune disorganization. Conversely, treated VL-HIV(T) patients exhibited increased connectivity and re-establishment of coordinated interactions between functional markers, indicating partial re-establishment of the MAIT cell immunological network architecture.
DISCUSSION: Together, VL and VL-HIV co-infection are associated with quantitative depletion and qualitative dysregulation of circulating MAIT cells, characterized by concurrent hyperactivation and exhaustion, coupled with immunological network fragmentation, while liposomal amphotericin B treatment appears to promote partial immunological reorganization.