Induction of antigen‐specific CD8+ cytolytic T cells by the exogenous bacterial antigen streptolysin O in rhesus monkeys

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Abstract
We have characterized the T cell responses induced by streptolysin O (SLO), a sulfydryl‐activated hemolysin secreted by streptococci, by applying long‐term in vitro culture and cloning rhesus monkey (Macaca mulatta) T cells. T cell lines specific for SLO were obtained from three rhesus monkeys. These T cell lines required autologous antigen‐presenting cells (APC) to proliferate in response to SLO and did not respond to purified protein derivative. Phenotypic analysis showed that the cells from two of three SLO‐specific T cell lines were more than 85% CD3+CD4−CD8+ after prolonged in vitro culture. The rh 1842 CD8+ T cell line proliferative response to SLO was inhibited by the addition of anti‐major histocompatibility complex (MHC) class I and anti‐CD8 but not of anti‐MHC class II and anti‐CD4 monoclonal antibody (mAb). This cell line was able to lyse P815 target cells in the presence of anti‐CD3 mAb and did not show natural killer activity. Moreover, specific lysis of autologous but not allogeneic non‐rosetting E− cell targets pulsed with SLO was observed. Such lysis was inhibited by the addition of anti‐MHC class I mAb. In the attempt to identify the restriction elements involved in SLO presentation APC from six unrelated rhesus monkeys and three humans were used. A CD4+ rh 1842 T cell clone responded when SLO was presented by one of six, and a CD8+ rh 1842 T cell clone by four of six rhesus monkeys APC. Both CD4+ and CD8+ T cell clones did not respond when SLO was presented by human APC. However, both clones responded when APC from all donors were used in conjunction with anti‐CD3 mb. Furthermore, SLO required active processing to be presented to CD4+ and CD8+ T cell clones as glutaraldehyde fixation of APC before but not after antigen pulsing inhibited T cell proliferation. The SLO‐specific CD8+ cytolytic T cells described here could play a role in the regulation of the immune response occurring during streptococcal infections and/or could participate in the pathogenesis of poststreptococcal nonsuppurative sequelae.