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Obesity enhances antiviral immunity in the genital mucosa through a microbiota-mediated effect on γδ T cells

ABSTRACT: Obesity enhances antiviral immunity in the genital mucosa through a microbiota-mediated effect on γδ T cells

PROVIDER: PRJNA830698 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18885469_1.fastq.gz	Fastqsanger.gz
	SRR18885469_2.fastq.gz	Fastqsanger.gz
	SRR18885470.fastq.gz	Fastqsanger.gz
	SRR18885471_1.fastq.gz	Fastqsanger.gz
	SRR18885471_2.fastq.gz	Fastqsanger.gz

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Obesity enhances antiviral immunity in the genital mucosa through a microbiota-mediated effect on γδ T cells

Project description:Obesity is detrimental to the immune system. It impairs lymphatics, T cell development, and lymphopoiesis; induces dysfunction of antitumor immunity; and also promotes tumor progression. However, direct evidence of the impact of obesity on viral infection is lacking. We found an unexpected protective role of obesity against herpes simplex virus 2 infection of the genital mucosa in mice. Although conventional antiviral immunity was comparable between obese mice and lean mice, obesity enhanced the cytotoxic subset of γδ T cells. This effect was mediated by L-arginine produced by commensal microbiota in the genital mucosa, which induced “pseudonormoxia” of γδ T cells, resulting in increased NKG2D expression of γδ T cells through the downregulation of HIF1A by inducing NO production, thereby protecting mice from lethal genital herpes. Thus, our work illuminates one mechanism by which obesity-induced compositional changes in the vaginal microbiota can affect mucosal immune responses against viral infection.

2023-07-12 | GSE201274 | GEO

Aging modifies endometrial dendritic cell function and unconventional double negative T cells in the human genital mucosa.

Project description:Immune function in the genital mucosa balances reproduction with protection against pathogens. As women age, genital infections, and gynecological cancer risk increase, however, the mechanisms that regulate cell-mediated immune protection in the female genital tract and how they change with aging remain poorly understood. Unconventional double negative (DN) T cells (TCRαβ + CD4-CD8-) are thought to play important roles in reproduction in mice but have yet to be characterized in the human female genital tract. Using genital tissues from women (27–77 years old), here we investigated the impact of aging on the induction, distribution, and function of DN T cells throughout the female genital tract.

2024-11-08 | GSE279408 | GEO

Mucosal CCL28 Chemokine Improves Protection against Genital Herpes through Mobilization of Antiviral Effector Memory CCR10+CD44+ CD62L-CD8+ T Cells and Memory CCR10+B220+CD27+ B Cells into the Infected Vaginal Mucosa

Project description:Four major mucosal-associated chemokines, CCL25, CCL28, CXCL14, and CXCL17, play an important role in protecting mucosal surfaces from infectious pathogens. However, their role in protection against genital herpes remains to be fully explored. The CCL28 is a chemoattractant for the CCR10 receptor-expressing immune cells and is produced homeostatically in the human vaginal mucosa (VM). In this study, we investigated the role of the CCL28/CCR10 chemokine axis in mobilizing protective antiviral B and T cell subsets into the VM site of herpes infection. We report a significant increase in the frequencies of HSV-specific memory CCR10+CD44+CD8+ T cells, expressing high levels of CCR10, in herpes-infected asymptomatic (ASYMP) women compared with symptomatic women. Similarly, a significant increase in the CCL28 chemokine (a ligand of CCR10), was detected in the VM of herpes-infected ASYMP C57BL/6 mice, associated with the mobilization of high frequencies of HSV-specific effector memory CCR10+CD44+CD62L-CD8+ TEM cells and memory CCR10+B220+CD27+ B cells in the VM of HSV-infected ASYMP mice. Inversely, compared with wild-type C57BL/6 mice, the CCL28 knockout (CCL28-/-) mice (1) appeared to be more susceptible to intravaginal infection and reinfection with HSV type 2, and (2) exhibited a significant decrease in the frequencies of HSV-specific effector memory CCR10+CD44+CD62L-CD8+ TEM cells and of memory CD27+B220+ B cells in the infected VM. These findings suggest a critical role of the CCL28/CCR10 chemokine axis in the mobilization of antiviral memory B and T cells within the VM to protect against genital herpes infection and disease.

2023-08-28 | GSE241702 | GEO

Expression data from mouse small intestinal γδ intraepithelial lymphocytes

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2011-04-06 | E-GEOD-28437 | biostudies-arrayexpress

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Breast cancer stem cell-derived tumors escape from γδ T cell immunosurveillance in vivo by modulating γδ T cell ligands

Project description:Triple negative breast cancer (TNBC) lacks targeted therapy options. TNBC is enriched in breast cancer stem cells (BCSCs), which play a key role in metastasis, chemoresistance, relapse and mortality. γδ T cells hold great potential in immunotherapy against cancer, and might be an alternative to target TNBC. γδ T cells are commonly observed to infiltrate solid tumors and have an extensive repertoire of tumor sensing, recognizing stress-induced molecules and phosphoantigens (pAgs) on transformed cells. We show that patient derived triple negative BCSCs are efficiently recognized and killed by ex vivo expanded γδ T cells from healthy donors. Orthotopically xenografted BCSCs, however, were refractory to γδ T cell immunotherapy. Mechanistically, we unraveled concerted differentiation and immune escape: xenografted BCSCs lost stemness, expression of γδ T cell ligands, adhesion molecules and pAgs, thereby evading immune recognition by γδ T cells. Indeed, neither pro-migratory engineered γδ T cells, nor anti-PD 1 checkpoint blockade significantly prolonged overall survival of tumor-bearing mice. BCSC immune escape was independent of the immune pressure exerted by the γδ T cells, and could be pharmacologically reverted by Zoledronate or IFN-α treatment. These results pave the way for novel combinatorial immunotherapies for TNBC.

2023-07-20 | PXD039463 | Pride

Gene expression profiling of oral and genital lichen planus epithelium and normal oral and genital epithelium

Project description:Comparing gene expression in Oral and genital lichen planus with normal oral and genital epithelium trying to idenitfy differently expressed genes in lichen planus compared to normal epithelium Total RNA obtained from oral and genital lichen planus epithelium compared with normal oral and genital epithelium

2013-11-08 | E-GEOD-52130 | biostudies-arrayexpress

Genital Tract Samples

Project description:Genital tract samples Raw

| PRJNA814891 | ENA

Gene expression profiling of oral and genital lichen planus epithelium and normal oral and genital epithelium

2013-11-08 | GSE52130 | GEO

PLA2G4A promotes right-sided colorectal cancer progression by inducing CD39+γδ Tregs polarization

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2022-02-17 | PXD027323 | Pride

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