The effect of an anti-HLA-B27 immune response on CTL recognition of Chlamydia

The interplay between triggering bacteria and HLA-B27 in the pathogenesis o f the spondyloarthropathies remains one of the most active areas of investi gation in the rheumatic diseases. This has proved difficult to study system atically in the clinical setting, and in this study we utilized a rat model to address the influence that B27-related immunity may have on the process of generating anti-Chlamydia immunity. When splenocytes from HLA-B27 DNA-i mmunized Lewis (LEW) animals received restimulation in vitro with Chlamydia -treated cells from B27-transgenic LEW rats, we observed that in addition t o the expected CTL recognition of HLA-B27, there was also anti-Chlamydia CT L killing of Chlamydia-sensitized syngeneic fibroblast targets. This was no t seen when responding cells in vitro were naive LEW splenocytes. To confir m the existence of CTLs recognizing both HLA-B27 and Chlamydia, LEW rats we re immunized with B27-transgenic LEW cells, instead of the B27 DNA construc t. Splenocytes from the immune rats were restimulated in vitro with Chlamyd ia-treated B27-transgenic LEW cells. In this instance, the CTLs retained th e allele-specific recognition of HLA-B27, as well as recognition of Chlamyd ia-sensitized syngeneic fibroblasts. Thus, if there is prior expansion of a n immune response against HLA-B27, then the resulting splenocytes demonstra te a reduced threshold for generating a primary anti-Chlamydia CTL response . These studies implicate a dynamic interrelationship between recognition o f HLA-B27 and Chlamydia trachomatis. The results may have implications for deciphering the cellular basis of Chlamydia-induced reactive arthritis.