scholarly journals Relative abilities of distinct isotypes of human major histocompatibility complex class II molecules to bind streptococcal pyrogenic exotoxin types A and B.

1992 ◽  
Vol 60 (12) ◽  
pp. 5025-5029 ◽  
Author(s):  
K Imanishi ◽  
H Igarashi ◽  
T Uchiyama
Keyword(s):  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Class ◽  
Class Ii ◽  
Complex Class ◽  
Major Histocompatibility ◽  
Human Major Histocompatibility Complex ◽  
Histocompatibility Complex

scholarly journals Expression of the Three Human Major Histocompatibility Complex Class II Isotypes Exhibits a Differential Dependence on the Transcription Factor RFXAP

2001 ◽  
Vol 21 (17) ◽  
pp. 5699-5709 ◽  
Author(s):  
Marie Peretti ◽  
Jean Villard ◽  
Emmanuèle Barras ◽  
Madeleine Zufferey ◽  
Walter Reith
Keyword(s):  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Class ◽  
Class Ii ◽  
Terminal Segment ◽  
Complex Class ◽  
Major Histocompatibility ◽  
Human Major Histocompatibility Complex ◽  
Histocompatibility Complex ◽  
Hla Dq ◽  
Mhcii Expression

ABSTRACT Major histocompatibility complex class II (MHCII) molecules play a pivotal role in the immune system because they direct the development and activation of CD4+ T cells. There are three human MHCII isotypes, HLA-DR, HLA-DQ, and HLA-DP. Key transcription factors controlling MHCII genes have been identified by virtue of the fact that they are mutated in a hereditary immunodeficiency resulting from a lack of MHCII expression. RFXAP—one of the factors affected in this disease—is a subunit of RFX, a DNA-binding complex that recognizes the X box present in all MHCII promoters. To facilitate identification of conserved regions in RFXAP, we isolated the mouse gene. We then delimited conserved domains required to restore endogenous MHCII expression in cell lines lacking a functionalRFXAP gene. Surprisingly, we found that 80% of RFXAP is dispensable for the reactivation of DR expression. Only a short C-terminal segment of the protein is essential for this isotype. In contrast, optimal expression of DQ and DP requires a larger C-terminal segment. These results define an RFXAP domain with an MHCII isotype-specific function. Expression of the three MHCII isotypes exhibits a differential requirement for this domain. We show that this is due to a differential dependence on this domain for promoter occupation and recruitment of the coactivator CIITA in vivo.

scholarly journals CTCF Controls Expression and Chromatin Architecture of the Human Major Histocompatibility Complex Class II Locus

2010 ◽  
Vol 30 (17) ◽  
pp. 4211-4223 ◽  
Author(s):  
Parimal Majumder ◽  
Jeremy M. Boss
Keyword(s):  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Class ◽  
Mhc Class Ii ◽  
Gene Promoter ◽  
Class Ii ◽  
Complex Class ◽  
Major Histocompatibility ◽  
Human Major Histocompatibility Complex ◽  
Mhc Ii ◽  
Histocompatibility Complex

ABSTRACT The major histocompatibility complex class II (MHC-II) locus includes a dense cluster of genes that function to initiate immune responses. Expression of insulator CCCTC binding factor (CTCF) was found to be required for expression of all MHC class II genes associated with antigen presentation. Ten CTCF sites that divide the MHC-II locus into apparent evolutionary domains were identified. To define the role of CTCF in mediating regulation of the MHC II genes, chromatin conformation capture assays, which provide an architectural assessment of a locus, were conducted across the MHC-II region. Depending on whether MHC-II genes and the class II transactivator (CIITA) were being expressed, two CTCF-dependent chromatin architectural states, each with multiple configurations and interactions, were observed. These states included the ability to express MHC-II gene promoter regions to interact with nearby CTCF sites and CTCF sites to interact with each other. Thus, CTCF organizes the MHC-II locus into a novel basal architecture of interacting foci and loop structures that rearranges in the presence of CIITA. Disruption of the rearranged states eradicated expression, suggesting that the formation of these structures is key to coregulation of MHC-II genes and the locus.

Sign in / Sign up

Export Citation Format

Share Document