AI Article Synopsis

  • Vγ6 γδ T cells, which primarily produce IL-17A, develop in the thymus during the perinatal stage.
  • A lack of MHC class II results in an increased number of IL-17A producing Vγ6 γδ T cells in the thymus.
  • This suggests that MHC class II plays a role in limiting the production of IL-17A Vγ6 γδ T cells during their development.

Article Abstract

Vγ6 γδ T cells develop in the thymus at the perinatal stage and are exclusive IL-17A producers among γδ T cells. The loss of MHC class II led to the expansion of IL-17A Vγ6 γδ T cells in the thymus. Thus, MHC class II in the thymus inhibits the generation of IL-17A Vγ6 γδ T cells.

Download full-text PDF

Source
http://dx.doi.org/10.1002/eji.202149542DOI Listing

Publication Analysis

Top Keywords

mhc class
12
il-17a vγ6
12
γδ cells
12
inhibits generation
8
generation il-17a
8
vγ6 γδ
8
cells thymus
8
thymus perinatal
8
perinatal stage
8
vγ6 γδ t
8

Similar Publications

Deep analysis of the major histocompatibility complex genetic associations using covariate analysis and haploblocks unravels new mechanisms for the molecular etiology of Elite Control in AIDS.

BMC Immunol

January 2025

Laboratoire Génomique, Bioinformatique, et Chimie Moléculaire, Conservatoire National des Arts et Métiers, 2 rue Conté 75003, Paris, EA7528, France.

Introduction: We have reanalyzed the genomic data from the International Collaboration for the Genomics of HIV (ICGH), focusing on HIV-1 Elite Controllers (EC).

Methods: A genome-wide association study (GWAS) was performed, comparing 543 HIV-1 EC individuals with 3,272 uninfected controls (CTR) of European ancestry. 8 million single nucleotide polymorphisms (SNPs) and HLA class I and class II gene alleles were imputed to compare EC and CTR.

View Article and Find Full Text PDF

Severe COVID-19 can trigger a cytokine storm, leading to acute respiratory distress syndrome (ARDS) with similarities to superantigen-induced toxic shock syndrome. An outstanding question is whether SARS-CoV-2 protein sequences can directly induce inflammatory responses. In this study, we identify a region in the SARS-CoV-2 S2 spike protein with sequence homology to bacterial super-antigens (termed P3).

View Article and Find Full Text PDF

Background: Concurrent (STK11, KL) mutant non-small cell lung cancers (NSCLC) do not respond well to current immune checkpoint blockade therapies, however targeting major histocompatibility complex class I-related chain A or B (MICA/B), could pose an alternative therapeutic strategy through activation of natural killer (NK) cells.

Methods: Expression of NK cell activating ligands in NSCLC cell line and patient data were analyzed. Cell surface expression of MICA/B in NSCLC cell lines was determined through flow cytometry while ligand shedding in both patient blood and cell lines was determined through ELISA.

View Article and Find Full Text PDF

Non-classical MHC class I genes which, compared to classical MHC class I, are typically less polymorphic and have more restricted expression patterns are attracting interest because of their potential to regulate immune responses to various pathogens. In salmonids, among the numerous non-classical MHC class I genes identified to date, L lineage genes, including Sasa- and , are differentially induced in response to microbial challenges. In the present study, we show that while transcription of both and are induced in response to SAV3 infection the transcriptional induction patterns are distinct for each gene.

View Article and Find Full Text PDF

Hypoimmune (HIP) allogeneic cell therapeutics hold the promise to allow off-the-shelf treatments for a broad patient population. Our HIP approach includes the depletion of major histocompatibility complex (MHC) class I and II molecules and the overexpression of Cd47. Here, we report the engineering of HIP mice that stably exhibit the HIP phenotype in all cell types.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!