PMID- 20192993
OWN - NLM
STAT- MEDLINE
DCOM- 20100520
LR  - 20211020
IS  - 1600-065X (Electronic)
IS  - 0105-2896 (Linking)
VI  - 233
IP  - 1
DP  - 2010 Jan
TI  - Role of HLA class II genes in susceptibility/resistance to inflammatory 
      arthritis: studies with humanized mice.
PG  - 62-78
LID - 10.1111/j.0105-2896.2009.00858.x [doi]
AB  - Predisposition to develop rheumatoid arthritis (RA) has been associated with 
      certain human leukocyte antigen (HLA) class II molecules, although the mechanism 
      is still unknown. Various experimental animal models of inflammatory arthritis 
      have been studied to address the role of major histocompatibility complex (MHC) 
      genes in pathogenesis. We have generated transgenic mice expressing HLA class II 
      molecules (DR and DQ) lacking complete endogenous class II molecules to study the 
      interactions involved between class II molecules (DQ and DR) and to define the 
      immunologic mechanisms in inflammatory arthritis. The HLA transgene can 
      positively select CD4(+) T cells expressing various V beta T-cell receptors, and 
      a peripheral tolerance is maintained to transgenic HLA molecules. The expression 
      of HLA molecules on various cells in these mice is similar to that known in 
      humans. In this review, we describe collagen-induced arthritis as a model for 
      human inflammatory arthritis using these transgenic mice. The transgenic mice 
      carrying RA-susceptible haplotype develop gender-biased inflammatory arthritis 
      with clinical and histopathological similarities to RA. Our studies show that 
      polymorphism of HLA class II genes determine the predisposition to 
      rheumatoid/inflammatory arthritis and the epistatic interactions between HLA-DQ 
      and HLA-DR molecules dictate the severity, progression, and modulation of the 
      disease.
FAU - Taneja, Veena
AU  - Taneja V
AD  - Department of Immunology, Mayo Clinic, Rochester, MN 55905, USA.
FAU - David, Chella S
AU  - David CS
LA  - eng
GR  - R01 AI075262/AI/NIAID NIH HHS/United States
GR  - R01 AR030752/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Review
PL  - England
TA  - Immunol Rev
JT  - Immunological reviews
JID - 7702118
RN  - 0 (Autoantibodies)
RN  - 0 (Epitopes)
RN  - 0 (HLA-DQ Antigens)
RN  - 0 (HLA-DR Antigens)
RN  - 29VT07BGDA (Citrulline)
RN  - 9007-34-5 (Collagen)
SB  - IM
MH  - Animals
MH  - Arthritis, Experimental/*genetics/immunology/prevention & control
MH  - Arthritis, Rheumatoid/*genetics/immunology/prevention & control
MH  - Autoantibodies/blood
MH  - B-Lymphocytes/immunology
MH  - Citrulline/immunology
MH  - Collagen/immunology
MH  - Epitopes
MH  - Female
MH  - Genetic Predisposition to Disease
MH  - HLA-DQ Antigens/*genetics/immunology
MH  - HLA-DR Antigens/*genetics/immunology
MH  - Humans
MH  - Male
MH  - Mice
MH  - Mice, Transgenic
MH  - Protein Processing, Post-Translational
MH  - Risk Assessment
MH  - Risk Factors
MH  - Sex Factors
MH  - T-Lymphocytes/immunology
RF  - 80
EDAT- 2010/03/03 06:00
MHDA- 2010/05/21 06:00
CRDT- 2010/03/03 06:00
PHST- 2010/03/03 06:00 [entrez]
PHST- 2010/03/03 06:00 [pubmed]
PHST- 2010/05/21 06:00 [medline]
AID - IMR858 [pii]
AID - 10.1111/j.0105-2896.2009.00858.x [doi]
PST - ppublish
SO  - Immunol Rev. 2010 Jan;233(1):62-78. doi: 10.1111/j.0105-2896.2009.00858.x.