CREB Regulates MHC Class II Expression in a CIITA-Dependent Manner

Moreno, Carlos S.; Beresford, Guy; Louis‐Plence, Pascale; Morris, Ann C.; Boss, Jeremy M.

doi:10.1016/s1074-7613(00)80015-1

Cited by 172 publications

(127 citation statements)

References 66 publications

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“…It has already been shown CIITA regulates MHC class II gene expression through directly affecting the gene promoters (Meissner et al, 2010;Staehli et al, 2012). Both MHC class I and MHC class II genes have a conserved WXY motif in their promoter regions (Moreno et al, 1999). As expected, ChIP assay indicated that NLRC5 associated with the MHC class I promoter in a similar manner as CIITA with MHC class II promoter (Meissner et al, 2010).…”

Section: Roles Of Nlrc5 In Regulating Immune Responses Nlrc5 Is a Massupporting

confidence: 64%

Expression regulation and function of NLRC5

Yao

Qian

2013

Protein Cell

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The NOD like receptors (NLRs), a class of intracellular receptors that respond to pathogen attack or cellular stress, have gained increasing attention. NLRC5, the largest member of the NLR protein family, has recently been identified as a critical regulator of immune responses. While NLRC5 is constitutively and widely expressed, it can be dramatically induced by interferons during pathogen infections. Both in vitro and in vivo studies have demonstrated that NLRC5 is a specifi c and master regulator of major mistocompatibility complex (MHC) class I genes as well as related genes involved in MHC class I antigen presentation. The expression of MHC class I genes is regulated by NLRC5 in coordination with the RFX components through an enhanceosome-dependent manner. And the involvement of NLRC5 in MHC class I mediated CD8 + T cell activation, proliferation and cytotoxicity is proved to be critical for host defense against intracellular bacterial infections. Nevertheless, the role of NLRC5 in innate immunity remains to be further explored. Here, we review the research advances on the structure, expression regulation and function of NLRC5.

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Section: Roles Of Nlrc5 In Regulating Immune Responses Nlrc5 Is a Massupporting

confidence: 64%

Expression regulation and function of NLRC5

Yao

Qian

2013

Protein Cell

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“…3, 6, 7, and 11-14). These include RFX, X2BP (cAMP response element binding protein; CREB), and NF-Y, which bind cooperatively to the X1 box (8,15), X2 box (8,9,16,17), and Y box (18,19), respectively. Together these proteins are engaged in the formation of a highly stable multiprotein DNA complex (20 -24).…”

Section: Novel Mutations Within the Rfx-b Gene And Partial Rescue Of mentioning

confidence: 99%

Novel Mutations Within the RFX-B Gene and Partial Rescue of MHC and Related Genes Through Exogenous Class II Transactivator in RFX-B-Deficient Cells

Nagarajan

Peijnenburg

Gobin

et al. 2000

The Journal of Immunology

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MHC class II deficiency or bare lymphocyte syndrome is a severe combined immunodeficiency caused by defects in MHC-specific regulatory factors. Fibroblasts derived from two recently identified bare lymphocyte syndrome patients, EBA and FZA, were found to contain novel mutations in the RFX-B gene. RFX-B encodes a component of the RFX transcription factor that functions in the assembly of multiple transcription factors on MHC class II promoters. Unlike RFX5- and RFXAP-deficient cells, transfection of exogenous class II transactivator (CIITA) into these RFX-B-deficient fibroblasts resulted in the induction of HLA-DR and HLA-DP and, to a lesser extent, HLA-DQ. Similarly, CIITA-mediated induction of MHC class I, β2-microglobulin, and invariant chain genes was also found in these RFX-B-deficient fibroblasts. Expression of wild-type RFX-B completely reverted the noted deficiencies in these cells. Transfection of CIITA into Ramia cells, a B cell line that does not produce a stable RFX-B mRNA, resulted in induction of an MHC class II reporter, suggesting that CIITA overexpression may partially override the RFX-B defect.

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“…The MHC class II (MHC-II) molecules are cell surface glycoproteins that are pivotal for inducing and regulating immune responses through their ability to present peptides derived from extracellular pathogens to CD4 + promoter, and the downstream X2 box is bound by the cyclic AMP response element-binding protein CREB [6][7][8][9]. The Y box binds the heterotrimeric transcription factor, NF-Y, which consists of A, B and C subunits [10,11].…”

Section: Introductionmentioning

confidence: 99%

Direct role of NF‐κB activation in Toll‐like receptor‐triggered HLA‐DRA expression

Lee

Kim

et al. 2006

Eur J Immunol

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Microbial components, such as DNA containing immunostimulatory CpG motifs (CpG-DNA) and lipopolysaccharides (LPS), elicit the cell surface expression of MHC class II (MHC-II) through Toll-like receptor (TLR)/IL-1R. Here, we show that CpG-DNA and LPS induce expression of the HLA-DRA in the human B cell line, RPMI 8226. Ectopic expression of the dominant negative mutant of CIITA and RNA interference targeting the CIITA gene indicate that CIITA activation is not enough for the maximal MHC-II expression induced by CpG-DNA and LPS. Additionally, nuclear factor (NF)-jB activation is required for the CpG-DNA-activated and LPS-activated HLA-DRA expression, whereas IFN-c-induced MHC-II expression depends on CIITA rather than on NF-jB. Comprehensive mutant analyses, electrophoretic mobility shift assays and chromatin immunoprecipitation assays, reveal that the functional interaction of NF-jB with the promoter element is necessary for the TLR-mediated HLA-DRA induction by CpG-DNA and LPS. This novel mechanism provides the regulation of MHC-II gene expression with complexity and functional diversity.

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CREB Regulates MHC Class II Expression in a CIITA-Dependent Manner

Cited by 172 publications

References 66 publications

Expression regulation and function of NLRC5

Expression regulation and function of NLRC5

Novel Mutations Within the RFX-B Gene and Partial Rescue of MHC and Related Genes Through Exogenous Class II Transactivator in RFX-B-Deficient Cells

Direct role of NF‐κB activation in Toll‐like receptor‐triggered HLA‐DRA expression

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