PMID- 18086265
OWN - NLM
STAT- MEDLINE
DCOM- 20080403
LR  - 20111117
IS  - 0001-2815 (Print)
IS  - 0001-2815 (Linking)
VI  - 71
IP  - 2
DP  - 2008 Feb
TI  - Evaluating the role of HLA-DQ polymorphisms on immune response to bacterial 
      superantigens using transgenic mice.
PG  - 135-45
AB  - Bacterial superantigens bind directly to human leukocyte antigen (HLA) class II 
      molecules and vigorously activate T cells expressing certain T-cell receptor 
      variable region families. As interaction with HLA class II molecules is the 
      primary step in this process, polymorphic variations in HLA class II can 
      determine the extent of superantigen binding to HLA class II molecules, govern 
      the magnitude of immune activation induced by given superantigens and determine 
      the outcome of superantigen-mediated diseases. As direct assessment of the 
      influence of HLA class II polymorphism in humans is impossible because of 
      expression of more than one HLA class II alleles in a given individual and 
      toxicity of superantigens, transgenic mice expressing HLA-DQ6 (HLA-DQA1*0103 and 
      HLA-DQB1*0601) and HLA-DQ8 (HLA-DQA1*0301 and HLA-DQB1*0302) were used to achieve 
      this goal. HLA-DQ6 and HLA-DQ8 elicited comparable in vitro and in vivo immune 
      response to staphylococcal enterotoxins (SE) A, SEB, SEH and SEK, toxic shock 
      syndrome toxin-1, streptococcal pyrogenic exotoxin (SPE) A and SPEC and 
      streptococcal mitogenic exotoxin Z (SMEZ). However, each superantigen had a 
      unique T-cell receptor activation profile. In vivo challenge with Streptococcus 
      pyogenes, H305, capable of elaborating SPEA and SMEZ, yielded a similar clinical 
      outcome in HLA-DQ6 and HLA-DQ8 transgenic mice. In conclusion, HLA-DQ6 and 
      HLA-DQ8 elicited comparable response to certain bacterial superantigens. Our 
      report highlights the advantages of HLA class II transgenic mice in such studies.
FAU - Rajagopalan, G
AU  - Rajagopalan G
AD  - Department of Immunology, Mayo Clinic College of Medicine, Mayo Clinic, 
      Rochester, MN 55905, USA. rajagopalan.govindarajan@mayo.edu
FAU - Polich, G
AU  - Polich G
FAU - Sen, M M
AU  - Sen MM
FAU - Singh, M
AU  - Singh M
FAU - Epstein, B E
AU  - Epstein BE
FAU - Lytle, A K
AU  - Lytle AK
FAU - Rouse, M S
AU  - Rouse MS
FAU - Patel, R
AU  - Patel R
FAU - David, C S
AU  - David CS
LA  - eng
PT  - Journal Article
DEP - 20071213
PL  - England
TA  - Tissue Antigens
JT  - Tissue antigens
JID - 0331072
RN  - 0 (HLA-DQ Antigens)
RN  - 0 (HLA-DQ6 antigen)
RN  - 0 (HLA-DQ8 antigen)
RN  - 0 (Superantigens)
SB  - IM
MH  - Animals
MH  - HLA-DQ Antigens/*genetics
MH  - Lymphocyte Activation/*genetics
MH  - Mice
MH  - Mice, Transgenic
MH  - Polymorphism, Genetic
MH  - Staphylococcus aureus/*immunology
MH  - Streptococcus pyogenes/*immunology
MH  - Superantigens/*immunology
MH  - T-Lymphocytes/immunology
EDAT- 2007/12/19 09:00
MHDA- 2008/04/04 09:00
CRDT- 2007/12/19 09:00
PHST- 2007/12/19 09:00 [pubmed]
PHST- 2008/04/04 09:00 [medline]
PHST- 2007/12/19 09:00 [entrez]
AID - TAN986 [pii]
AID - 10.1111/j.1399-0039.2007.00986.x [doi]
PST - ppublish
SO  - Tissue Antigens. 2008 Feb;71(2):135-45. doi: 10.1111/j.1399-0039.2007.00986.x. 
      Epub 2007 Dec 13.