The immune response to Porphyromonas gingivalis, one of the key pathogens in periodontitis etiology, was analyzed activating naïve CD4+ T cells from healthy individuals with autologous dendritic cells pulsed with different P. gingivalis serotypes.Whereas serotypes K1 or K2 triggered a Th1/Th17 response, serotypes K3, K4 or K5 triggered a Th2 response, and K- a Treg phenotype. We found a good correlation between the secreted cytokines and expression of the master switch transcription factors T-bet and RORC2 in response to K1 or K2, or with GATA-3 and the secreted cytokines in response to K3-K5. However, there was no correlation between expression of Foxp3 and secretion of IL-10 or TGF-β1 on response to K-. In addition, T cells responding to K1 or K2, but not to the other serotypes led to an increased secretion of RANKL, a key cytokine involved in bone metabolism. Although the data could not be simply explained by differences in the frequency of T cells able to respond to the different serotypes on healthy and periodontitis affected individuals, it allowed to link serotypes K1 and K2 to the Th1/Th17 response and bone resorption characteristic of periodontitis.

This work has been supported by grants from the Spanish Ministry of Science and Education (SAF2007-63631 to JAGS) and the Spanish Ministry of Health (FIS-060181 to MS). RV is recipient of a CONICYT-26080046 fellowship from the Chilean Government.

46 p.-2 tab.-7 fig.-1 fig S

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