The association between Actinobacillus actinomycetemcomitans (Aa) and aggressive periodontitis is well documented. Moreover, a recent study showed that Aa was able to induce apoptosis of human T-cells and that the Aa-GroEL was involved (Nalbant et al., Oral Micro Immunol, 2003). Heat shock proteins (HSPs), like GroEL, are known to be immunodominant in some oral and nonoral diseases; they are not typically inhibitory. Objective: Our long-term goal is to characterize the T-cell response to the HSPs from Aa in mice and in human periodontitis patients. Methods: Genes encoding Aa-HSPs, GroEL, GroES, and DNAJ, were cloned and recombinant proteins were produced. The purified HSPs were tested for the ability to stimulate both T-cell hybridomas generated from Aa-inoculated mice and PBCs from patients with aggressive periodontitis. Results: Of the murine T-cell hybridomas tested, 3 recognized GroES and 1 was stimulated by GroEL. Although a response was seen in mice, none of these HSPs was able to stimulate proliferation of human T-cells. However, the lack of T-cell reactivity may have been due to the absence of active Aa in the periodontium of these individuals. More importantly, the recombinant proteins, including GroEL, were not inhibitory. The human T-cells proliferated well to mitogenic stimulus, even in the presence of Aa GroEL. In addition, the inhibitory effect of Aa on human T-cells was heat labile, suggesting the existence of a toxic factor in Aa that is distinct from GroEL. Conclusion: The HSPs GroES and GroEL were identified as T-cell epitopes in our murine hybridoma model. The lack of proliferation to the same Aa antigens in human subjects may indicate variability in host T-cell responses or that recent Aa-exposure is necessary. Importantly, recombinant GroEL alone was not inhibitory. (This work was supported by NIDCR grant DE12952).

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