In conclusion, the results of the present study suggested that upregulation of IL-21 and IL-10 and downregulation LBH589 of IL-4

in periodontitis tissues may be collectively involved in the increased levels of salivary IgA in chronic periodontitis subjects. Since only cytokine profiles and salivary IgA level were evaluated and, no characterization of naïve B cell switch in the periodontal lesions was performed, these preliminary findings are still not enough to definitely define the mechanisms of Ig isotype switching on chronic periodontitis. However, our results may provide new insights into the possible role of Th-secreted cytokines in driving humoral immune response on periodontal tissue breakdown. The authors thank Ms Jeruza P. Bossonaro for technical assistance and São Paulo State Research Foundation (São Paulo, São Paulo, Brazil) for its financial support (# 2008/09687-0; # 2008/04280-0). “
“This chapter contains sections titled: The immune system Tissues and

cells of the immune system Activation, regulation and functions of immune responses Innate versus adaptive immunity Primary and secondary immune responses Immune cell development Mast cells and basophils Eosinophils Neutrophils Monocytes and macrophages Dendritic cells Natural killer cells CD4+ T helper cells CD8+, cytotoxic T cells B cells γδ T cells Seliciclib in vitro Natural killer T cells Anatomy of the immune system Lymph nodes Spleen Summary “
“Although Fasudil has shown therapeutic potential in EAE mice, the mechanism of action are still not fully understood. Here, we examined the immunomodulatory effect of Fasudil on encephalitogenic mononuclear cells (MNCs), and tested the therapeutic

potential of Fasudil-treated MNCs in active EAE. Fasudil inhibited expression of CCL20 on T cells and migration of T cells, decreased CD4+IFN-γ+ and CD4+IL-17+ T cells, but increased CD4+IL-10+ and CD4+TGF-β+ Cyclin-dependent kinase 3 T cells. Fasudil reduced expression of CD16/32 and IL-12, while elevating expression of CD206, CD23, and IL-10. Fasudil also decreased levels of iNOS/NO, enhanced levels of Arg-1, and inhibited the TLR-4/NF-κB signaling and TNF-α, shifting M1 macrophage to M2 phenotype. These modulatory effects of Fasudil on T cells and macrophages were not altered by adding autoantigen MOG35–55 to the culture, i.e., autoantigen-independent. Further, we observed that, in vitro, Fasudil inhibited the capacity of encephalitogenic MNCs to adoptively transfer EAE and reduced TLR-4/p-NF-κB/p65 and inflammatory cytokines in spinal cords. Importantly, Fasudil-treated encephalitogenic MNCs exhibited therapeutic potential when injected into actively induced EAE mice. Together, our results not only provide evidence that Fasudil mediates the polarization of macrophages and the regulation of T cells, but also reveal a novel strategy for cell therapy in MS.