In Mycobacterium tuberculosis, the FtsZ C-terminus mediates the interaction between FtsZ and FtsW. EzrA and SepF are Gram-positive division proteins that modulate FtsZ. The effects of EzrA or SepF on FtsZ polymerization can be relieved by adding competing amounts of a synthetic peptide encoding the FtsZ C-terminus, and EzrA and SepF have no effects on a C-terminal truncation mutant of FtsZ that still polymerizes. The SepF study showed that SepF bundles FtsZ filaments and co-sediments with FtsZ in polymerization experiments. The FtsZBsD16 truncate still polymerized but no longer bundled in the presence of SepF, yet SepF still co-sedimented with FtsZBsD16. This hypothesis is currently supported by the intermittent occurrence of ruptures in the nuclear envelope in dermal fibroblast cultures of patients carrying selected LMNA mutations. These ruptures are accompanied by the loss of cellular compartmentalization. The sequestration of sumo1 within mutant lamin aggregates paralleled with an increase in the steady-state levels of sumoylated proteins in nuclear extracts of C2C12 cells. There was also a modest increase in the amount of non-conjugated sumo1. By contrast, IL-4 and IFN- levels showed a significant reduction in patients with CP, as compared to those of healthy gingival samples, while other studies demonstrated an increase in IL-4 and IL-6 after treatment, suggesting a protective role for these cytokines. In most studies evaluating DCs in periodontal disease, an increase in these cells can be observed in diseased tissues, as compared to healthy samples, although a decrease in the later processes of the disease can also be seen. In the present study, positive correlations could be identified between immature DCs and probing depth. Likewise, fewer immature DCs could be found in the group of individuals with advanced CP. Although no comparisons were performed between diseased tissue and NM, these data indicate that increased numbers of immature DCs are associated with the initial stage of periodontal disease. In addition, negative correlations could be observed between immature DCs and CAL.3, as well as between immature DCs and CAL.5, thus suggesting that these cells decrease with the severity of CP. The present study found an increase in the percentage of sites with PD.4 and CAL.3, and IL-6 levels and immature DCs with higher inflammatory infiltrate. In a previous study by our research group, an increase in immature DCs with inflammatory infiltrate was identified, while mature DCs proved to be positively correlated with mild inflammatory infiltrate in samples presenting chronic gingivitis. In this study, a decrease in mature DCs, with higher inflammatory infiltrate, could be observed. This observation was also associated with the absence of these cells in the SE, a region characterized by intense inflammatory infiltrate in the adjacent LP. Therefore, the inverse relation of mature DCs with inflammatory infiltrate may well explain their absence in the SE. In conclusion, the IL-6 can contribute to the increase of the immature DCs in the CP, in turn impacting the inflammatory response. Higher levels of IL-2, TNF-a, INF-, IL-10, and IL-17A cytokines in the gingival tissue are related to human CP.