Streptococcal cell wall arthritis. Passive transfer of disease with a T cell line and crossreactivity of streptococcal cell wall antigens with Mycobacterium tuberculosis.

Abstract

Primary lymph node cells derived from streptococcal cell wall arthritic rats or those derived from adjuvant arthritic rats proliferated in response to cell wall antigens derived from either streptococcal cell walls or those from M. tuberculosis. In addition, two T cell lines have been isolated from lymph nodes of rats during the chronic phase of streptococcal cell wall arthritis. These T cell lines transfered clinical disease to naive syngeneic irradiated recipients, and they proliferated in the presence of cell wall antigens derived from streptococci or antigens derived from Mycobacterium but failed to proliferate in the presence of the 65-kD antigen (containing the sequence TFGLQLELT) derived from Mycobacterium. These observations indicate that T cells play a crucial role in the pathogenesis of streptococcal cell wall arthritis and suggest that antigenic crossreactivity exists between cell walls of group A streptococci and antigens derived from Mycobacterium. The 65-kD Mycobacterium protein is not involved in the observed antigenic crossreactivity.

Tranilast Suppresses the Disease Development of the Adjuvant- and Streptococcal Cell Wall-Induced Arthritis in Rats

“…What was so interesting was that in the acute phase of the SIA model, tranilast was measured to exceed the performance of MTX. This observation presumably lies in the differences between the pathologies of the two models; the acute phase reaction of SIA is a complement-dependent T cell-independent pathology, whereas T cells are essential for the reactivation in the chronic phase (22). Thus, it is likely that T cell-dependent phases are susceptible to MTX and MTX's major cellular target is T cells (22).…”

“…The similarities and differences between AIA and SIA are well known. In T cells, the antigenic cross-reactivity between components of the streptococcal cell wall and mycobacterial antigens have been reported (22); whereas the AIA disease process is monophasic and eventually remits, SIA is biphasic and persistent. In addition, the AIA process is entirely T celldependent, while in the SIA model, the acute phase is T cell-independent (23).…”

Gut flora induces and maintains resistance against streptococcal cell wall-induced arthritis in F344 rats

“…However, functional T lymphocytes have been shown to play a pivotal role in suseeptibility to SCWinduced, chronic joint inflammation; there even is evidence that SCW-specific T cells are required [3][4][5][6][8][9][10][11]17], Thus, an answer to the question why T cells from F344 rats do not respond to SCW after priming with cell walls might elucidate the mechanism of resistance to SCW arthritis.…”

“…Together, these data strongly suggest an absolute dependence on functional T lymphocytes of the ehronic phase of SCW-induced arthritis. An ultimate proof for the crucial involvement of T cells and even a hint to SCW-induced arthritis being an autoimmune disease came from adoptive transfer experiments in SCW-induced arthritis [8], In addition, we have described a correlation Correspondence: Maries F, van den Broek, Autoimmune Diseases, Central Laboratory of the Netherlands Red Cross Blood Transfusion Service, Pleomarclaan 125, 1066 CX Amsterdam, The Netherlands, between susceptibility to chronic SCW-induced arthritis and the ability to mount SCW-specific T cell responses [9,10], Prevention ofthe development of SCW-specific T cells in Lewis rats, for instance by pretreatment with the mycobacterial 65-kD heat shock protein [11] or with small amounts of eell walls (unpublished results), results in resistance to SCW-indueed arthritis. Moreover, treatment of Lewis rats with MoAbs against CD4 makes Lewis rats completely refractory to SCW-induced arthritis [20] and induces a long-term tolerance to SCW, coinciding with long-term resistance to SCW-induced arthritis.…”

Rheumatoid Arthritis: Laboratory Models of the Disease

“…Модель реактивации использована для исследо-вания экспрессии генов в суставных тканях [43] и для генотерапии [32]. С человеческим РА дан-ный вид артрита роднит смена спонтанных ре-миссий и обострений хронического воспаления [12].…”