| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Departments of
*
Immunology and
Rheumatology, Mayo Clinic and Medical School, Rochester, MN 55905; and
Research Service, Veteran’s Affairs Medical Center, and Department of Medicine, Division of Rheumatology, University of Utah, Salt Lake City, UT 84132
We have generated transgenic (tg) mice expressing HLA-DQ8
ß
(DQA1*0301/DQB*0302) or HLA-DQ6ß
(DQA1*0103/DQB1*0601) molecules lacking endogenous
murine class II expression (Aß0) to investigate the ability of these
HLA class II to present type II collagen (CII) and induce
collagen-induced arthritis. The DQ8ß tg mice responded strongly to
CII, developing severe arthritis, while DQ6ß tg mice were
nonresponsive to CII. The addition of the mixed haplotype DQ86ß
molecule did not significantly influence CII reactivity. To examine the
interaction of DQ6ß and DQ8ß molecules in vivo, we generated
double tg DQ6ß/8ß (Aß0) mice expressing both the - and
ß-chains of DQ6 and DQ8 molecules by mating DQ6ß (Aß0) and
DQ8ß (Aß0) tg mice. CII-immunized DQ6ß/8ß tg mice
developed severe experimental polychondritis, exhibiting both
polyarthritis and auricular chondritis. The clinical, serologic, and
histologic manifestations of experimental polychondritis are similar to
those symptoms in human relapsing polychondritis. The susceptibility of
DQ6ß/8ß tg mice compared with resistance in the parental
strains suggests that expression of both the DQ6ß and DQ8ß
tgs, unique to the DQ6ß8ß tg strain, is important in
susceptibility to experimental polychondritis. The DQ6ß/8ß tg
mice provide a model to investigate putative autoantigens and the
mechanisms of pathogenesis involved in relapsing polychondritis as well
as the influence of the expression of multiple HLA class II molecules
on the disease process.
This article has been cited by other articles:
|
|
 |
|
  M. Kitagaki and M. Hirota Auricular Chondritis Caused by Metal Ear Tagging in C57BL/6 Mice Vet. Pathol., July 1, 2007; 44(4): 458 - 466. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A.-S. Hansson, M. Johannesson, L. Svensson, K. S. Nandakumar, D. Heinegard, and R. Holmdahl Relapsing Polychondritis, Induced in Mice with Matrilin 1, Is an Antibody- and Complement-Dependent Disease Am. J. Pathol., March 1, 2004; 164(3): 959 - 966. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. A. Taylor, E. Havari, M. F. McInerney, R. Bronson, K. W. Wucherpfennig, and M. A. Lipes A Spontaneous Model for Autoimmune Myocarditis Using the Human MHC Molecule HLA-DQ8 J. Immunol., February 15, 2004; 172(4): 2651 - 2658. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Wen, F. S. Wong, J. Tang, N.-Y. Chen, M. Altieri, C. David, R. Flavell, and R. Sherwin In Vivo Evidence for the Contribution of Human Histocompatibility Leukocyte Antigen (HLA)-DQ Molecules to the Development of Diabetes J. Exp. Med., January 3, 2000; 191(1): 97 - 104. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. J. Krco, S. Watanabe, J. Harders, M. M. Griffths, H. Luthra, and C. S. David Identification of T Cell Determinants on Human Type II Collagen Recognized by HLA-DQ8 and HLA-DQ6 Transgenic Mice J. Immunol., August 1, 1999; 163(3): 1661 - 1665. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
