ArticleThe Journal of experimental medicine1997
An isotype-specific activator of major histocompatibility complex (MHC) class II genes that is independent of class II transactivator.
Article in The Journal of experimental medicine, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 33 citations in OpenAlex.
- Suppressive and pro-inflammatory roles for IL-4 in the pathogenesis of experimental drug-induced liver injury: a review.Expert opinion on drug metabolism & toxicology · 2010Review
- An MHC class II restriction bias in CD4 T cell responses toward I-A is altered to I-E in DM-deficient mice.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- Patterns of constitutive and IFN-gamma inducible expression of HLA class II molecules in human melanoma cell lines.Immunogenetics · 2007Article
- Impact of human cytomegalovirus latent infection on myeloid progenitor cell gene expression.Journal of virology · 2004Article
- Differential major histocompatibility complex class II locus expression on human laryngeal epithelium.Clinical and experimental immunology · 2003Article
- Class II transactivator: mastering the art of major histocompatibility complex expression.Molecular and cellular biology · 2000Review
- Novel mutants define genes required for the expression of human histocompatibility leukocyte antigen DM: evidence for loci on human chromosome 6p.The Journal of experimental medicine · 1997Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Patients with one type of major histocompatibility complex class II combined immunodeficiency have mutations in a gene termed class II transactivator (CIITA), which coordinately controls the transcription of the three major human class II genes, HLA-DR, -DQ, and -DP. However, the experimentally derived B-lymphoblastoid cell line, clone 13, expresses high levels of HLADQ in the absence of HLA-DR and HLA-DP, despite its mapping by complementation analysis to this group. It was possible that one of the clone 13 CIITA alleles bore a mutation that allowed HLA-DQ, but not HLA-DR or -DP transcription. Alternatively, another factor, distinct from CIITA, might control HLA-DQ expression. We report here that ectopic expression of CIITA cDNAs derived by reverse transcriptase polymerase chain reaction from clone 13 do not restore expression of HLA-DQ in another CIITA-deficient cell line, RJ2.2.5. In addition, no CIITA protein is detectable in clone 13 nuclear extracts. In contrast, somatic cell fusion between clone 13 and RJ2.2.5 restored expression of the HLA-DQ haplotype encoded by the RJ2.2.5 DQB gene. Taken together, these data demonstrate the existence of an HLA-DQ isotype-specific trans-acting factor, which functions independently of CIITA.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.