Immunity to heat shock proteins and arthritic disorders

Eden, Willem van

doi:10.1002/(sici)1098-0997(1999)7:1/2<49::aid-idog10>3.0.co;2-e

Cited by 5 publications

(1 citation statement)

References 20 publications

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“…It seems appropriate to designate this refractory state as ‘tolerance’, because pretreated, sensitized donors are unable to transfer disease, whereas adoptive transfer of sensitized cells from untreated donors produces AD equally readily in MT‐treated and normal recipients. van Eden and his colleagues have worked out the molecular events underlying resistance of this type in great detail [27, 41, 42]. The pathogenic peptide HSP65 p180–188 itself can serve as a protective ligand.…”

Section: Adjuvant Disease: Regulationmentioning

confidence: 99%

Immune Regulation in Adjuvant Disease and Other Arthritis Models: Relevance to Pathogenesis of Chronic Arthritis

Waksman

2002

Scand J Immunol

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Experimental models of arthritis and their human counterparts fall into three distinct classes: (a) responses of T cells to disseminated microbial antigens (Ags) as such; (b) responses of T cells to cartilage autoAgs; and (c) responses of T cells to major histocompatibility complex (HLA‐B27, DRB1) or other membrane components (LFA‐1) expressed on bone marrow‐derived cells. The primary immune response is driven, in naturally occurring disease, by microbial infection, e.g. with streptococci, enteric gram‐negative rods or spirochetes, or is experimentally induced with mycobacterial and other adjuvants. The response to cartilage components, such as collagen type‐II and various proteoglycans, may be driven by cross‐reactive microbial Ags, heat shock proteins (HSPs) in particular, or the adjuvant effect of intense primary joint inflammation, as in rheumatoid arthritis and the spondyloarthropathies. Adjuvant disease appears to be purely T‐cell‐mediated, whereas both T cells and antibody play a role in collagen and many other forms of arthritis. Experimental evidence suggests a pathogenetic role for T‐cell receptor γδ T cells in some lesions. Arthritis may be regulated by microbial and tissue HSPs, when these are administered by a nonimmunizing route or as altered peptide ligands, by anti‐idiotypic responses that block the action of effector T cells, and by competing Ags. Immune regulation involving natural killer (NK), NK T and certain subsets of γδ and αβ T cells, which may affect the occurrence, localization and character of this group of diseases, presents a challenge for further investigation.

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Section: Adjuvant Disease: Regulationmentioning

confidence: 99%