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Selection of evolutionarily conserved mucosal-associated invariant T cells by MR1
It is shown that T cells that express the canonical hVα7.2-Jα33 or mVα19-J α33 TCR rearrangement are preferentially located in the gut lamina propria of humans and mice, respectively, and are therefore genuine mucosal-associated invariant T (MAIT) cells.
A cluster of ten novel MHC class I related genes on human chromosome 6q24.2-q25.3.
Human RAET1 products are all devoid of the membrane-proximal immunoglobulin-like alpha3 domain and most, but not all, are predicted to remain membrane-anchored via glycosylphosphatidylinositol linkage and are shown to display an atypical pattern of polymorphism.
Delirium and encephalopathy in severe COVID-19: a cohort analysis of ICU patients
TheDelirium/neurological symptoms in COVID-19 patients were responsible for longer mechanical ventilation compared to the patients without delirium or abnormal neurological symptoms, and could be secondary to systemic inflammatory reaction to SARS-CoV-2.
Mutations in signal recognition particle SRP54 cause syndromic neutropenia with Shwachman-Diamond–like features
Shwachman-Diamond syndrome (SDS) (OMIM #260400) is a rare inherited bone marrow failure syndrome (IBMFS) that is primarily characterized by neutropenia and exocrine pancreatic insufficiency.
Lipolysis is altered in MHC class I zinc-alpha(2)-glycoprotein deficient mice.
In contrast to previously reported data, ZAG was found to be ubiquitously and constitutively expressed, with an especially high level in the mouse liver, and no overt immunological phenotype was identified in these animals.
Inactivation of the hemochromatosis gene differentially regulates duodenal expression of iron-related mRNAs between mouse strains.
The up-regulation of these transcripts suggests that an inappropriate iron-deficiency signal is sensed by the duodenal enterocytes, leading to an enhanced ferric reductase activity and the increase of duodental iron uptake and transfer to the circulation.
A basolateral sorting motif in the MICA cytoplasmic tail
The physiological location of MICA within epithelial cells is governed by its cytoplasmic tail, implying impairment in A5.1 homozygous individuals, perhaps relevant to the immunological surveillance exerted by NK and T lymphocytes on epithelial malignancies.