Divergent evolution in the mechanisms controlling major histocompatibility complex class II gene transcription in mouse and human

Barbaro, Andrea De Lerma; Rigaud, Gildas; Sartoris, Silvia; Nicolis, Morena; Cestari, Tiziana; Accolla, Roberto S.

doi:10.1002/eji.1830260140

Cited by 4 publications

(5 citation statements)

References 22 publications

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“…This result is explained by the segregation of one copy of human autosome 6 at the time of RP3-7.6 hybrid clone RNA preparation (data not shown). The remaining HLA-DQB1 and -DQA1 alleles give rise to the single 1.2-kb band of corresponding mRNA, as previously shown [24].…”

Section: Differential Re-expression Of Human Class I1 Genes In Psu1 Xsupporting

confidence: 73%

“…The following mAb were used: K22.42.2, specific for I-E antigens; and 25.9.17, specific for I-A antigens. These antibodies do not cross-react with human HLA class I1 antigens [24]. The FITC series of histograms represent the control staining of the various cell populations after incubation with irrelevant, isotype-matched first antibody followed by the rabbit anti-mouse FITC-labeled antibodies: M12.4.1, mouse B cell lymphoma; P3-U1, mouse plasmacytoma; P3-CII-3, mouse P3-U1 transfected with CIITA; RP3-7, Raji X P3-U1 interspecies hybrid; and RP3-7.6, R/P3-7 transfected with CIITA.…”

Section: Aansfection With Human Ciita Results In De Novo Expression Omentioning

confidence: 92%

“…Drastically reduced cell surface expression of DQ molecules in the hybrids, in presence of normal cell surface expression of HLA-DR and -DP, correlated with absence of detectable mature HLA-DQaP heterodimers not only at the cell surface but also in the intracellular pool. Normal amounts of specific HLA-DQa and -DQp transcripts were nevertheless present [24]. The data currently available do not allow to establish whether the lack of HLA-DQaP heterodimers is due to lack of translation or inappropriate assembling of the a and P subunits.…”

Section: Discussionmentioning

confidence: 92%

“…Flow cytofluorometric analysis of the RP3-7 hybrid, its derived NP3-7.6 CIITA-transfected clone, and corresponding human (Raji) and mouse (P3-U1) parental cells, after incubation with mAb specific for the human MHC class I1 antigens listed in the top of the histograms, followed by staining with the rabbit anti-mouse FITC-labeled antibodies. The following mAb were used: D1-12, specific for D R antigens; B7/21, specific for D P antigens; BT 3/4, specific for DQ1 antigens; and XI11 358.4, specific for DQ2 antigens [24]. These antibodies do not cross-react with mouse MHC class I1 antigens.…”

Section: Dna and Rna Analysismentioning

confidence: 99%

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Active suppression of the class II transactivator‐encoding AIR‐1 locus is responsible for the lack of major histocompatibility complex class II gene expression observed during differentiation from B cells to plasma cells

Sartoris

Tosi²,

Barbaro³

et al. 1996

Eur J Immunol

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In this study the genetic control of major histocompatibility complex (MHC) class II gene expression during the transition from B cell to plasma cell has been analyzed. Class II molecules are not expressed in plasma cells because of an active suppression resulting in the abrogation of class II gene transcription. We show here that the plasma cell-specific repressor function, designated SIR (suppressor of immune response genes), does not act directly on the transcription of class II genes, but instead on the transcription of the AIR-1 gene, whose product, the class II transactivator (CIITA), is fundamental for the regulation of the constitutive and inducible expression of MHC class II genes. This was unambiguously demonstrated by the fact that plasmacytoma x B cell hybrids carrying an AIR-1 locus derived from CIITA-expressing cells do not express CIITA-specific transcripts. Transfection of a cDNA containing the human CIITA coding sequence under the control of an heterologous promoter restores expression of human MHC class II genes in the hybrids and is responsible for de novo expression of mouse MHC class II genes in both the mouse plasmacytoma cell line and the hybrids. These results confirm and extend the notion of the functional conservation of the AIR-1 gene product across species barriers. Interestingly, in CIITA-transfected cell hybrids, cell surface expression of the human HLA-DQ heterodimer was not observed. This result was not attributable to lack of HLA-DQ alpha or -DQ beta transcription, because both transcripts were present in the CIITA-transfected hybrids, although at reduced levels. These findings further support our previous observations on the distinct regulation of expression of the human HLA-DQ class II subset, which may be thus controlled at the posttranscriptional level by a CIITA-independent mechanism.

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Section: Differential Re-expression Of Human Class I1 Genes In Psu1 Xsupporting

confidence: 73%

Section: Aansfection With Human Ciita Results In De Novo Expression Omentioning

confidence: 92%

Section: Discussionmentioning

confidence: 92%

Section: Dna and Rna Analysismentioning

confidence: 99%

See 2 more Smart Citations

Active suppression of the class II transactivator‐encoding AIR‐1 locus is responsible for the lack of major histocompatibility complex class II gene expression observed during differentiation from B cells to plasma cells

Sartoris

Tosi²,

Barbaro³

et al. 1996

Eur J Immunol

Self Cite

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“…In the mouse there is limited evidence of locus-specific control of transcription. Thus in binding of factors to the X box, H-2Aa is the odd man out among H-2Aa, H-2Ea and H-2EP (74); while in the rescue of human class I1 expression within mouse x human cell hybrids, it is H-2Ea (75). There exist also locus-specific post-transcriptional ' control mechanisms, which distinguish between DQ versus DR and DP (76).…”

Section: Mhc Class II Promoter Structure and Functionmentioning

confidence: 99%

Functional significance of polymorphism among MHC class II gene promoters

et al. 1996

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The functional significance of polymorphism among MHC class II promoters in man and mouse is here reviewed, mainly in terms of the hypothesis of differential expression. The hypothesis proposes that differences between antigen-presenting cells in MHC class II expression exert a co-dominant effect on the Th1-Th2 cytokine balance, such that class II molecules of one type come to control to a greater extent the production of one group of cytokines, and those of another type the production of the alternative group. The survey deals with the influence of signal strength and antigen-presenting cell type on T-cell subset differentiation; functional differences between MHC class II molecules not obviously related to determinant selection; disease protection mediated by HLA alleles; mechanisms possibly responsible for allotypic and isotypic bias; overdominance (heterozygous advantage) in selection for expression of class II alleles; MHC class II promoter structure and function; inter-locus and inter-allele variability within human MHC class II gene upstream regulatory regions; a comparison of these polymorphisms in mouse and man; read-out of class II promoter function; and a comparison with expression of MHC class I. We conclude that the evidence that this variation is functionally active (i.e. controls expression) is increasing, but is not yet compelling. The crucial test still to come, we suggest, is whether or not the biological effects attributable to this polymorphism will line up with molecular studies on expression.

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MHC class II gene regulation: some historical considerations on a still ontogenetic and phylogenetic puzzle

Accolla

Tosi²,

Sartoris³

et al. 1999

Microbes and Infection

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Divergent evolution in the mechanisms controlling major histocompatibility complex class II gene transcription in mouse and human

Cited by 4 publications

References 22 publications

Active suppression of the class II transactivator‐encoding AIR‐1 locus is responsible for the lack of major histocompatibility complex class II gene expression observed during differentiation from B cells to plasma cells

Active suppression of the class II transactivator‐encoding AIR‐1 locus is responsible for the lack of major histocompatibility complex class II gene expression observed during differentiation from B cells to plasma cells

Functional significance of polymorphism among MHC class II gene promoters

MHC class II gene regulation: some historical considerations on a still ontogenetic and phylogenetic puzzle

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