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Skin Resident Memory CD4+ T Cells Enhance Protection Against Leishmania Major Infection

ABSTRACT: Leishmaniasis causes a significant disease burden worldwide. Although Leishmania-infected patients become refractory to reinfection following disease resolution, effective immune protection has not yet been achieved by human vaccines. While circulating Leishmania-specific T cells are known to play a critical role in immunity, the role of memory T cells present in peripheral tissues has not been explored. Here, we identify a population of skin-resident Leishmania-specific memory CD4+ T cells. These cells produce IFNγ, and remain resident in the skin when transplanted by skin graft onto naïve mice. They function to recruit circulating T cells to the skin in a CXCR3 dependent manner, resulting in better control of the parasites. Our findings are the first to demonstrate that CD4+ TRM cells form in response to a parasitic infection, and indicate that optimal protective immunity to Leishmania, and thus the success of a vaccine, may depend on generating both circulating and skin-resident memory T cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE69998 | GEO | 2015/06/19

SECONDARY ACCESSION(S): PRJNA287436

REPOSITORIES: GEO

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Skin Resident Memory CD4+ T Cells Enhance Protection Against Leishmania Major Infection

Project description:Leishmaniasis causes a significant disease burden worldwide. Although Leishmania-infected patients become refractory to reinfection following disease resolution, effective immune protection has not yet been achieved by human vaccines. While circulating Leishmania-specific T cells are known to play a critical role in immunity, the role of memory T cells present in peripheral tissues has not been explored. Here, we identify a population of skin-resident Leishmania-specific memory CD4+ T cells. These cells produce IFNγ, and remain resident in the skin when transplanted by skin graft onto naïve mice. They function to recruit circulating T cells to the skin in a CXCR3 dependent manner, resulting in better control of the parasites. Our findings are the first to demonstrate that CD4+ TRM cells form in response to a parasitic infection, and indicate that optimal protective immunity to Leishmania, and thus the success of a vaccine, may depend on generating both circulating and skin-resident memory T cells. Two conditions were analyzed. For each condition, four mice were used, resulting in eight samples in total.

2015-06-19 | E-GEOD-69998 | biostudies-arrayexpress

Transcriptional control of influenza-specific CD4+ tissue-resident memory T cell generation

Project description:Tissue-resident memory T cells (TRM) are a non-circulating subset of memory that are maintained at sites of pathogen entry and mediate optimal protection against reinfection. Lung TRM can be generated in response to respiratory infection or vaccination, however, the molecular pathways involved in CD4+TRM establishment have not been defined. Here, we performed transcriptional profiling of influenza-specific lung CD4+TRM following influenza infection to identify pathways implicated in CD4+TRM generation and homeostasis. Lung CD4+TRM displayed a unique transcriptional profile distinct from spleen memory, including up-regulation of a gene network induced by the transcription factor IRF4, a known regulator of effector T cell differentiation.

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2023-01-30 | E-MTAB-11116 | biostudies-arrayexpress

Mus musculus

Project description:Skin Resident Memory CD4+ T Cells Enhance Protection Against Leishmania Major Infection

| PRJNA287436 | ENA

single cell RNA sequencing of CD8+CD44+GP33+ T cells from spleen and intraepithelial lymphocytes from small intestine at day 30 post LCMV Arm infection

Project description:During acute infections, CD8+ T cells form various memory subpopulations to provide long-lasting protection against reinfection. Central memory (TCM), Effector memory (TEM), and long-lived effector (LLE) cells are circulating memory populations with distinct plasticity, migration patterns, and effector functions. Tissue-resident memory (TRM) cells permanently reside in the frontline sites of pathogen entry and provide tissue-specific protection upon reinfection. Here, using scRNA-seq and bulk RNA-seq, we examined the different and shared transcriptomes and regulators of TRMs with other circulating memory populations. Furthermore, we identified heterogeneity within the TRM pool from small intestine and novel transcriptional regulators that may control the phenotypic and functional heterogeneity of TRM cells during acute infection. Our findings provide a resource for future studies to identify novel pathways for enhancing vaccination and immunotherapeutic approaches.

2021-08-31 | GSE181784 | GEO

Bulk RNA sequencing of TCM, TEM, and TRM from CD8+CD44+GP33+ T cells after LCMV infection

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Expression data from circulating and lung tissue resident memory CD4 T cell responding towards infuenza A virus infection

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Human resident memory T cells exit the skin and mediate systemic Th2-driven inflammation.

Project description:To investigate the transcriptional profile of human circulating T cells with skin tissue-resident memory phenotype (cTRM) in GVHD we performed bulk RNA sequencing from SMART-seq2 of sorted human cTRM (CD3+ CD4+ CLA+ CD103+) and conventional T cells (CD3+ CD4+ CD103-), and single cell RNA sequencing from 10X Genomics of sorted human CD45+, both from isolated blood PBMCs of patients with active acute GVHD.

2021-09-24 | GSE183212 | GEO

Genomic profiling of human Leishmania braziliensis lesions identifies transcriptional modules associated with cutaneous immunopathology

Project description:The host immune response plays a critical role not only in protection from human leishmaniasis, but also in promoting disease severity. Although candidate gene approaches in mouse models of leishmaniasis have been extremely informative, a global understanding of the immune pathways active in lesions from human patients is lacking. To address this issue, genome-wide transcriptional profiling of Leishmania braziliensis-infected cutaneous lesions and normal skin controls was carried out. A signature of the L. braziliensis skin lesion was defined that includes over 2,000 differentially regulated genes. Pathway-level analysis of this transcriptional response revealed key biological pathways, as well as specific genes, associated with cutaneous pathology, generating a testable 'metapathway' model of immune-driven lesion pathology, and providing new insights for treatment of human leishmaniasis. Thirty-five skin biopsies were analyzed, including 10 normal skin biopsies (2 from North America and 8 from non-endemic area in Brazil), and 25 skin lesion biopsies (8 early cutaneous lesions, 17 late cutaneous lesions) obtained from Leishmania brazilensis-infected patients presenting at the Corte de Pedra Health Post in Corte de Pedra, Bahia, Brazil.

2014-03-07 | E-GEOD-55664 | biostudies-arrayexpress

Leishmania major modulates autophagy in host macrophages during intracellular differentiation

Project description:Autophagy generally participates in innate immunity by elimination of intracellular pathogens. However, many of them developed successful strategies to counteract their autolysosomal digestion and lastly to exploit this catabolic cellular process. Protozoan parasites of the genus Leishmania are the causative agent of leishmaniasis, one of the 13 most important tropical diseases. Leishmania persists as endo-parasite in host macrophages, where it uses multiple strategies to manipulate the microbicidal host cell functions and to escape from the host immune system. Understanding how Leishmania interacts with host macrophages during uptake, differentiation, intracellular replication, and release might be the key to develop new drugs in target-directed approaches to treat patient with leishmaniasis. Here, we generated expression profiles from bone marrow-derived macrophages (BMDM) at 1h and 24h post infection (p.i.) with Leishmania major and respective controls.

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