Katalog Plus
Bibliothek der Frankfurt UAS
Bald neuer Katalog: sichern Sie sich schon vorab Ihre persönlichen Merklisten im Nutzerkonto: Anleitung.
Dieses Ergebnis aus BASE kann Gästen nicht angezeigt werden.  Login für vollen Zugriff.

Phenotype, functional properties, and gut recruitment of CX3CR1+ effector lymphocytes in HIV-1-infected individuals on antiretroviral therapy ; Caractérisation des lymphocytes effecteurs CX3CR1+ et de leur recrutement intestinal au cours de l'infection VIH-1 sous traitement antirétroviral

Title: Phenotype, functional properties, and gut recruitment of CX3CR1+ effector lymphocytes in HIV-1-infected individuals on antiretroviral therapy ; Caractérisation des lymphocytes effecteurs CX3CR1+ et de leur recrutement intestinal au cours de l'infection VIH-1 sous traitement antirétroviral
Authors: Collercandy, Nived
Contributors: Institut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity); Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Toulouse (EPE UT); Communauté d'universités et établissements de Toulouse (Comue de Toulouse)-Communauté d'universités et établissements de Toulouse (Comue de Toulouse); Université de Toulouse; Pierre Delobel
Source: https://theses.hal.science/tel-05419204 ; Médecine humaine et pathologie. Université de Toulouse, 2025. Français. ⟨NNT : 2025TLSES127⟩.
Publisher Information: CCSD
Publication Year: 2025
Collection: Université Toulouse III - Paul Sabatier: HAL-UPS
Subject Terms: Gut; CX3CL1; CX3CR1; Lymphocytes; HIV-1; Intestin; Microenvironnement; Lymphocytes effecteurs mémoires; VIH-1; [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology; [SDV.IMM]Life Sciences [q-bio]/Immunology
Description: The gut is a major site of viral reservoir persistence during HIV-1 infection, which stands as an obstacle toward the reach of HIV remission. This reservoir is associated with an incomplete restoration of T CD4+ lymphocytes locally, a gut-barrier dysfunction, and an increase of bacterial translocation and local inflammation, despite effective prolonged antiretroviral therapy.Effector cellular immune response is crucial for infection control. HIV-1 induces a loss of intestinal resident memory lymphocytes and an increase in blood cells with a gut-tropic recirculating profile. CX3CR1-CX3CL1 axis may be a key to the recruitment of tissular effector cells but seem to be impacted by the chronic HIV-1 infection, even under ART, with an increase of circulating CX3CR1+ cells and an increase in soluble CX3CL1 in the plasma. Here, we aimed to characterize the effector CX3CR1+ cells in both the blood and the gut, search for environmental factors that could modulate this chemotactic axis and assess the impact of this axis modulation in the gut viral reservoir in a cohort of people living with HIV (PLWH) under long term ART.In a first work on γδ Vδ1 T cells, which frequencies were increased in the blood of PLWH, we highlighted the clonal expansion of a highly cytotoxic effector population of Vδ1 expressing CX3CR1 with a recirculating cell-like phenotype. This population correlated with HIV-1 infection reduction in the associated blood or duodenal compartment. We showed that cytomegalovirus (CMV) residual replication during HIV-1 infection was a major trigger for CX3CR1+ CD8 and Vδ1 T cells expansion, but this effect was in an interplay of tissular microbiome changes that were also associated with CMV.In a second work, we showed that CX3CR1+ CD8 T cells were increased in frequency in both the blood and the gut. However, in the colon this increase was associated with a loss of resident memory CX3CR1+ CD8 T cells with higher effector functions. This population was associated with lower viral reservoir, especially for with the ...
Document Type: doctoral or postdoctoral thesis
Language: French
Relation: NNT: 2025TLSES127
Availability: https://theses.hal.science/tel-05419204; https://theses.hal.science/tel-05419204v1/document; https://theses.hal.science/tel-05419204v1/file/2025TLSES127.pdf
Rights: https://about.hal.science/hal-authorisation-v1/ ; info:eu-repo/semantics/OpenAccess
Accession Number: edsbas.4C9367B7
Database: BASE