Regulation of MHC Class II Gene Expression

Reith, Walter; Steimle, Viktor; Durand, Bénédicte; Kobr, Michel; Mach, Bernard

doi:10.1016/s0171-2985(11)80550-4

Cited by 18 publications

(19 citation statements)

References 21 publications

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“…The primary regulation of class II molecule expression is at the level of transcription, which is both cell type and development stage specific (11,17,58,68,70). Our work demonstrates that the increase in MHC class II expression on HTLV-1-transformed T cells is due to an increase in the level of MHC class II mRNA.…”

Section: Discussionmentioning

confidence: 68%

“…1A, compare lanes 4 and 5). In contrast, transcription factor YB-1, which has also been shown to bind to the Y box of the MHC class II promoter (58,68,70,84), failed to bind to either GST or GST-Tax (Fig. 1A, lanes 6 and 7).…”

Section: Resultsmentioning

confidence: 95%

“…The functional consequence of this variation is the regulation and restriction of the cellular immune response, since the structure of each class II molecule determines which peptide sequences are presented to lymphoid cells (58,68,70). The MHC class II-peptide complexes determine the repertoire of mature T cells and the activation of CD4 ϩ T cells and thus play a fundamental role in the homeostasis of the immune response.…”

Section: Discussionmentioning

confidence: 99%

“…The MHC class II promoters share conserved sequence motifs, which include the W, X, X2, and Y boxes. Nuclear factors which bind to these sequences have been identified, and some have been cloned (17,68,70,84). Reports have shown that binding of the factors which control the class II promoter is cooperative and that NF-Y binding facilitates in vivo recruitment of upstream transcription factors (69,84).…”

Section: Discussionmentioning

confidence: 99%

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Physical and Functional Interaction between the Human T-Cell Lymphotropic Virus Type 1 Tax₁ Protein and the CCAAT Binding Protein NF-Y

Pise-Masison

Dittmer

Clemens

et al. 1997

Molecular and Cellular Biology

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Human T-cell lymphotrophic virus type 1 (HTLV-1) is the causative agent of the aggressive, usually fatal adult T-cell leukemia (see references 22, 23, 48 and 86 and references therein). Recent reports have linked HTLV-1 with additional and clinically diverse human diseases (31,46,53,59,63,65). The best characterized of these is a progressive demyelinating syndrome termed HTLV-1-associated myelopathy (HAM) or tropical spastic paraparesis (TSP) (see references 22, 23, 48, and 86 and references therein). Because of the long incubation period between viral exposure and disease onset, the mechanism of HTLV-1 pathogenesis is still unclear. It is clear that host cell control of HTLV-1 replication is a primary determinant of virus expression and subsequent disease. Studies on the variation of viral sequences among different infected groups have not revealed any particular determinant which distinguishes onset of a particular HTLV-1 associated disease (18,44,60,74,87,88).In vitro, HTLV-1 has been shown to activate and immortalize human T lymphocytes, resulting in the polyclonal proliferation of infected cells and subsequent oligoclonal or monoclonal growth (26, 43). HTLV-1 contains no known cellular protooncogene, and because there is no preferential site of integration among infected individuals, it is unlikely that insertional mutagenesis is responsible for viral transformation. Several lines of evidence suggest that the viral transcriptional activator Tax contributes to the development of disease (23,28,29,82).Tax, which is essential for viral replication (22,23,48,86), has recently been shown to transform established rodent fibroblasts to anchorage-independent growth (77, 82, 85). Moreover, Tax can transform primary rat embryo fibroblasts in cooperation with activated ras (67) as well as immortalize normal human T lymphocytes when expressed from a herpes simplex virus-based vector (28,29). Finally, transgenic mice carrying the Tax gene frequently develop mesenchymal tumors and neurofibromas (34, 62). These findings suggest that Tax plays a critical role in HTLV-1-associated leukemogenesis.Tax is believed to exert its effect by stimulating viral gene expression and by deregulating expression of cellular genes (22,23,48,86). Tax has been shown to activate transcription of a number of cellular genes involved in cell proliferation, such as those for interleukin-3 (IL-3), IL-2, the IL-2 receptor, granulocyte-macrophage colony-stimulating factor, c-Fos, c-Jun, parathyroid-related protein, and the major histocompatibility complex (MHC) class I (see references 22, 23, 48, and 86 and references therein). The aberrant expression of these growthrelated genes has been implicated in contributing to the establishment of HTLV-1-associated pathogenesis. While Tax does not bind DNA directly, it appears to stimulate RNA synthesis through protein-protein interactions with host cell transcription factors. The most well studied of these interactions is with the ATF/CREB family of transcription factors, which bind to cyclic AMP-responsive...

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Section: Discussionmentioning

confidence: 68%

Section: Resultsmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Physical and Functional Interaction between the Human T-Cell Lymphotropic Virus Type 1 Tax₁ Protein and the CCAAT Binding Protein NF-Y

Pise-Masison

Dittmer

Clemens

et al. 1997

Molecular and Cellular Biology

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“…MHC class II gene expression in immune cells are regulated by two factors known as CIITA and a Y box-binding protein [43,44]. CIITA is a non-DNA-binding protein transactivator that functions as a molecular switch to control constitutive and IFNg-inducible MHC class II gene expression in immune cells [44±49].…”

Section: Discussionmentioning

confidence: 99%

IFNγ/TNFα synergism in MHC class II induction: effect of nicotinamide on MHC class II expression but not on islet-cell apoptosis

Kim

Chang

et al. 2002

Diabetologia

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Differential expression of insulin‐dependent diabetes mellitus‐associated HLA‐DQA1 alleles in vivo

et al. 1997

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The strong association of HLA-DQ genes with insulin-dependent diabetes mellitus (IDDM) susceptibility is persuasive evidence of their central role in the etiology of this autoimmune disease. Among other possibilities, it has been proposed that an unbalanced expression of IDDM-associated DQA, and/or DQB alleles may lead to alterations in the composition of alpha beta heterodimers and preferential expression of a particular heterodimer on the antigen-presenting cell surface, leading to self-recognition. In this report, we demonstrate the differential expression of DQA1 alleles in vivo, in particular of the two diabetogenic alleles DQA1*0301 and DQA1*0501. Family studies suggest that unequal HLA-DQA1 allele expression in heterozygous individuals is not associated in cis with the HLA-DQA1 gene, but may be affected by trans-acting determinant(s). We also discuss the segregation of this phenotype in IDDM-affected members. Furthermore, we examined historical samples of PBL from an IDDM-affected individual and an HLA-identical unaffected sibling acting in a kidney transplant program as donor and recipient, respectively. This analysis allowed us to establish that unbalanced expression of DQA1*0301 and DQA1*0501 can be induced by microenvironmental conditions. Inducible differential expression of HLA-DQA1 alleles may account for the discordance in the outcome of autoimmune disease in monozygotic twins and HLA-identical siblings.

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Regulation of MHC Class II Gene Expression

Cited by 18 publications

References 21 publications

Physical and Functional Interaction between the Human T-Cell Lymphotropic Virus Type 1 Tax₁ Protein and the CCAAT Binding Protein NF-Y

Physical and Functional Interaction between the Human T-Cell Lymphotropic Virus Type 1 Tax₁ Protein and the CCAAT Binding Protein NF-Y

IFNγ/TNFα synergism in MHC class II induction: effect of nicotinamide on MHC class II expression but not on islet-cell apoptosis

Differential expression of insulin‐dependent diabetes mellitus‐associated HLA‐DQA1 alleles in vivo

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Regulation of MHC Class II Gene Expression

Cited by 18 publications

References 21 publications

Physical and Functional Interaction between the Human T-Cell Lymphotropic Virus Type 1 Tax1 Protein and the CCAAT Binding Protein NF-Y

Physical and Functional Interaction between the Human T-Cell Lymphotropic Virus Type 1 Tax1 Protein and the CCAAT Binding Protein NF-Y

IFNγ/TNFα synergism in MHC class II induction: effect of nicotinamide on MHC class II expression but not on islet-cell apoptosis

Differential expression of insulin‐dependent diabetes mellitus‐associated HLA‐DQA1 alleles in vivo

Contact Info

Product

Resources

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Physical and Functional Interaction between the Human T-Cell Lymphotropic Virus Type 1 Tax₁ Protein and the CCAAT Binding Protein NF-Y

Physical and Functional Interaction between the Human T-Cell Lymphotropic Virus Type 1 Tax₁ Protein and the CCAAT Binding Protein NF-Y