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Cytolytic γδ T-cells and IFNγ-producing CD4-lymphocytes characterise the early response to MTBVAC tuberculosis vaccine

ABSTRACT: In this work, we performed in-depth analyses of the immune populations proliferating 7 days after encounter with MTBVAC. We found that CD4+ and gd T cells were the main populations expanded.

ORGANISM(S): Homo sapiens

PROVIDER: GSE268279 | GEO | 2025/03/28

REPOSITORIES: GEO

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Cytolytic γδ T-cells and IFNγ-producing CD4-lymphocytes characterise the early response to MTBVAC tuberculosis vaccine

Project description:Cytolytic γδ T-cells and IFNγ-producing CD4-lymphocytes characterise the early response to MTBVAC tuberculosis vaccine

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Macrophage-Targeted Therapy Unlocks Antitumoral Cross-talk between IFNγ-Secreting Lymphocytes and IL12-Producing Dendritic Cells.

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Phenotypic Characterization of Porcine IFNγ-Producing Lymphocytes in Porcine Reproductive and Respiratory Syndrome Virus Vaccinated and Challenged Pigs.

Project description:Porcine reproductive and respiratory syndrome (PRRS) continues to be one of the most important swine diseases worldwide. Interferon-γ (IFNγ)-mediated type I cell-mediated immune response plays an important role in protection from, and clearance of, PRRS virus (PRRSV). Several lymphocyte subsets including T-helper, CTLs, Th/memory cells, and γδ T lymphocytes were previously reported to produce IFNγ during PRRSV infection. However, the proportion and phenotypic characterization of these IFNγ-secreting lymphocytes have not been explored. In this study, IFNγ producted by different lymphocyte subsets was assessed by multi-color flow cytometry after vaccination with PRRSV modified live vaccine (PRRSV-MLV) and challenge with homogeneous or heterogeneous PRRSV. The results showed that T-helper cells were the major IFNγ-secreting cell population after PRRSV-MLV vaccination and PRRSV challenge. Additionally, the proportion of IFNγ producing Th/memory cells and γδ T cells increased after PRRSV challenge. This difference was accounted for an enhanced ability to produce IFNγ in Th/memory cells and an enlarged quantity of γδ T cells. The results presented here could contribute to our understanding of the roles of IFNγ in protective immunity against PRRSV infection and may be useful for assessment of cell-mediated immunity in vaccine tests.

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Human γδ T cells in diverse tissues exhibit site-specific maturation dynamics across the life span

Project description:Early in ontogeny, gd T cells emerge from the thymus and directly seed peripheral tissues for in situ immunity, though their function in human tissues is not clear. Through analysis of gd T cells in mucosal and lymphoid tissues across the human lifespan, we reveal age- and site-specific differentiation states, functions, and dynamics. Pediatric tissues uniquely contain newly generated gd T cells with diverse repertoires, exhibiting tissue repair and effector functions. In adult tissues, gd T cells persist in lower frequencies, exhibiting highly expanded repertoires and cytolytic profiles. Over childhood, gd T cells convert to adult-like differentiation profiles in mucosal sites, revealing that gd T cells provide diverse recognition and functions for numerous antigenic challenges during early life but persist as terminally differentiated, innate-like cells thereafter.

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Project description:Interleukin (IL)-17A is a cytokine originally reported to induce neutrophil-mediated inflammation and anti-microbial activity. The CD4(+) T cells, which produce IL-17A, have been well characterized as Th17 cells. On the other hand, IL-17A-producing TCR γδ(+) T cells have been reported to participate in the immune response at an early stage of infection with Listeria monocytogenes and Mycobacterium bovis in mice. However, the involvement of IL-17A in protective immunity was not clearly demonstrated in the chronic stage of M. tuberculosis-infected mice.We analyzed role of IL-17A in host defense against chronically infected M. tuberculosis using IL-17A KO mice.We found that TCR γδ(+) T cells are a primary source of IL-17A, but that mycobacterial antigen-specific Th17 cells were hardly detected even at the chronic stage of M. tuberculosis infection. IL-17A-deficient mice showed a decreased survival rate, and increased bacterial burden in the lungs after the infection when compared to the wild-type mice. Furthermore, a histological analysis showed an impaired granuloma formation in the infected lungs of IL-17A-deficient mice, which was considered to be due to a decrease of IFN-γ and TNF at the chronic stage.Our data suggest that the IL-17A-producing TCR γδ(+) T cells, rather than the Th17 cells, in the infected lungs are an indispensable source of protective immunity against M. tuberculosis infection.

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A Macrophage Colony-Stimulating Factor-Producing gamma-delta T Cell Subset Prevents Malarial Parasitemic Recurrence

Project description:Despite evidence that gd T cells play an important role during malaria, their precise role remains unclear. During murine malaria induced by Plasmodium chabaudi infection and in human P. falciparum infection, we found that gd T cells expanded rapidly after resolution of acute parasitemia, in contrast to ab T cells that expanded at the acute stage and then declined. Single-cell sequencing showed that TRAV15N-1 gd T cells were clonally expanded in mice and had convergent complementarity-determining region 3 sequences. These gd T cells expressed specific cytokines, M-CSF, CCL5, CCL3, which are known to act on the myeloid compartment, indicating that this gd T cell subset may have distinct functions. Both gd T cells and M-CSF were necessary for preventing parasitemic recurrence. These findings point to an M-CSF-producing gd T cell subset that fulfills a specialized protective role in the later stage of malaria infection when ab T cells have declined.

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Project description:Helicobacter pylori is a gram-negative bacterium that causes gastric and duodenal diseases in humans. Despite a robust antibody and cellular immune response, H. pylori infection persists chronically. To understand if and how H. pylori could modulate T cell activation, in the present study we investigated in vitro the interaction between H. pylori and human T lymphocytes freshly isolated from peripheral blood of H. pylori-negative donors. A direct interaction of live, but not killed bacteria with purified CD3+ T lymphocytes was observed by microscopy and confirmed by flow cytometry. Live H. pylori activated CD3+ T lymphocytes and predominantly γδ+ T cells bearing the TCR chain Vδ2. Upon interaction with H. pylori, these cells up-regulated the activation molecule CD69 and produced cytokines (such as TNFα, IFNγ) and chemokines (such as MIP-1β, RANTES) in a non-antigen-specific manner. This activation required viable H. pylori and was not exhibited by other gram-negative bacteria. The cytotoxin-associated antigen-A (CagA), was at least partially responsible of this activation. Our results suggest that H. pylori can directly interact with T cells and modulate the response of γδ+ T cells, thereby favouring an inflammatory environment which can contribute to the chronic persistence of the bacteria and eventually to the gastric pathology.

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