ArticleThe Journal of experimental medicine1994
Class II transactivator (CIITA) is sufficient for the inducible expression of major histocompatibility complex class II genes.
Article in The Journal of experimental medicine, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers.
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Who cites it
118 citing papers in PubMed, 329 citations in OpenAlex.
- IRF-4-mediated CIITA transcription is blocked by KSHV encoded LANA to inhibit MHC II presentation.PLoS pathogens · 2013Trial
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- New insights into the structure domain and function of NLR family CARD domain containing 5.Cell communication and signaling : CCS · 2025Review
- MDM2 inhibitors in cancer immunotherapy: Current status and perspective.Genes & diseases · 2024Review
- Untangling the genetics of beta cell dysfunction and death in type 1 diabetes.Molecular metabolism · 2024Review
- Timing of whole genome duplication is associated with tumor-specific MHC-II depletion in serous ovarian cancer.Nature communications · 2024Article
- Association of CIITA (rs8048002) and CLEC2D (rs2114870) gene variants and type 1 diabetes mellitus.Journal of diabetes and metabolic disorders · 2024Article
- Unraveling the transcriptomic landscape of eye migration and visual adaptations during flatfish metamorphosis.Communications biology · 2024Article
- The NLR gene family: from discovery to present day.Nature reviews. Immunology · 2023Review
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- Cellular and molecular dynamics in the lungs of neonatal and juvenile mice in response toeLife · 2023Article
- Convergence of YAP/TAZ, TEAD and TP63 activity is associated with bronchial premalignant severity and progression.Journal of experimental & clinical cancer research : CR · 2023Article
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- Identification of IL-27 as a novel regulator of major histocompatibility complex class I and class II expression, antigen presentation, and processing in intestinal epithelial cells.Frontiers in immunology · 2023Article
- Inhibition of the CtBP complex and FBXO11 enhances MHC class II expression and anti-cancer immune responses.Cancer cell · 2022Article
58 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The class II transactivator (CIITA) has been shown to be required for major histocompatibility complex (MHC) class II gene expression in B cells and its deficiency is responsible for a hereditary MHC class II deficiency. Here we show that CIITA is also involved in the inducible expression of class II genes upon interferon gamma (IFN-gamma) treatment. The expression of CIITA is also inducible with IFN-gamma before the induction of MHC class II mRNA. In addition, CIITA mRNA expression does not require new protein synthesis, although new protein synthesis is necessary for the transcription of class II. This suggests that synthesis of new CIITA protein may be essential to induce class II gene expression. We also showed that the JAK1 protein tyrosine kinase activity is required to induce the expression of CIITA upon IFN-gamma stimulation. This finding indicates that CIITA is part of the signaling cascade from the IFN-gamma receptor to the activation of class II genes. In addition, the expression of CIITA is sufficient to activate class II genes in the absence of IFN-gamma stimulation suggesting that CIITA is the major regulatory factor for the inducible expression of class II genes. Together, these data suggest that CIITA is the IFN-inducible cycloheximide sensitive factor previously shown to be required for the induction of MHC class II gene expression.
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