       Document 0004
 DOCN  M9620004
 TI    Pathogenesis of spondylarthropathies. Persistent bacterial antigen,
       autoimmunity, or both?
 DT    9602
 AU    Sieper J; Braun J; Klinikum Benjamin Franklin, Free University of
       Berlin, Germany.
 SO    Arthritis Rheum. 1995 Nov;38(11):1547-54. Unique Identifier : AIDSLINE
       MED/96062427
 AB    We have discussed partially mutually exclusive, partially overlapping
       models for the pathogenesis of the spondylarthropathies. Not all
       possibilities have been presented here; others are discussed elsewhere
       (77, 78). Furthermore, we have not addressed the issue of B27-negative
       spondylarthropathy. However, in our opinion, the key to understanding
       the pathogenesis of the spondylarthropathies lies in the interaction
       between the class I MHC molecule HLA-B27 and the T cell response.
       Although a T cell response driven by persisting bacterial antigen is
       still an attractive hypothesis, it does not explain all the known
       aspects of spondylarthropathy pathogenesis. The possibility of
       autoimmunity triggered by bacterial infection needs also to be
       considered, especially the new idea of HLA-B27-derived peptides
       presented by class II MHC molecules. The predominant involvement of
       joints is not easily explained in the case of autoimmunity.
       Cross-reactivity to joint-specific structures such as type II collagen
       (79) and/or bacteria inside the joint at the beginning of the immune
       response, with induction of local autoimmunity, might be involved. Most
       of the issues raised here could be tested by experiment, and we can
       expect to learn soon whether any of these models will explain the
       pathogenesis, or if we have to look further. The PCR technique will
       facilitate the search for bacteria not only in peripheral joints, but
       also now in sacroiliac biopsy samples from patients with AS and other
       spondylarthropathies. A prospective study on ReA in an endemic area
       should teach us more about predisposing factors (for example for
       Shigella-induced enteritis, which occurs in many parts of the world
       outside Europe and the US) (80).(ABSTRACT TRUNCATED AT 250 WORDS)
 DE    Antigen Presentation  Antigens, Bacterial/IMMUNOLOGY  Autoimmunity
       CD8-Positive T-Lymphocytes/IMMUNOLOGY  Human  Joint
       Diseases/*ETIOLOGY/IMMUNOLOGY  Spinal Diseases/*ETIOLOGY/IMMUNOLOGY
       Support, Non-U.S. Gov't  JOURNAL ARTICLE  REVIEW  REVIEW, TUTORIAL

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

