ArticleFrontiers in immunology2022
A Spontaneous H2-Aa Point Mutation Impairs MHC II Synthesis and CD4
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- IL-27 producers in a neonatal BCG vaccination model are a heterogenous population of myeloid cells that are diverse in phenotype and function.ImmunoHorizons · 2025Article
- CD4-Derived Double-Negative T Cells Ameliorate Alzheimer's Disease-Like Phenotypes in the 5×FAD Mouse Model.CNS neuroscience & therapeutics · 2025Article
- Transcriptomic analysis of liver immune response in Chinese spiny frog (Open life sciences · 2024Article
- The effect of FMT and vitamin C on immunity-related genes in antibiotic-induced dysbiosis in mice.PeerJ · 2023Article
- The H2-A Class II molecule α/β-chainFrontiers in immunology · 2023Article
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Major histocompatibility complex class II (MHC II) is an essential immune regulatory molecule that plays an important role in antigen presentation and T-cell development. Abnormal MHC II expression can lead to immunodeficiency, clinically termed as type II bare lymphocyte syndrome (BLS), which usually results from mutations in the MHC II transactivator (CIITA) and other coactivators. Here, we present a new paradigm for MHC II deficiency in mice that involves a spontaneous point mutation on H2-Aa. A significantly reduced population of CD4
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