The immunology of dermatophytosis is Butylhydroxyanisole currently poorly understood. Some works have focused on T cell immunity against dermatophytes. It is now accepted that a cell-mediated immune response is responsible for the control of infection by dermatophytes. On the other hand, susceptibility to chronic dermatophytosis is associated with atopy and with immediate type hypersensitivity. Dendritic cells are located at sites of antigen exposure as the mucosa and peripheral tissues. The precursors of these cells originate in the bone marrow and migrate to constantly various tissues such as skin, the gastrointestinal, respiratory, blood and lymph. In peripheral tissues, these cells are inefficient in antigen presentation and activation of T cells, because they have immature phenotype. Immature dendritic cells have low expression of co-stimulatory molecules and molecules of MHC class I and II but have large phagocytic capacity. Tregs activation is involved in the prevention of rejection, the induction and maintenance of peripheral Tubeimoside-I tolerance of the allograft, and the support of allograft survival. Several other studies indicated that Tregs are an essential element of the immunoregulatory pathway which induces peripheral allograft tolerance, that the frequency of circulating Tregs is significantly decreased during acute rejection, and that the transfer of Tregs pre-stimulated in vitro can protect skin and cardiac allografts from acute and chronic rejection. In clinical transplantation, T cells with the phenotypic characteristics of regulatory cells are detected in both the peripheral blood and within the graft itself. In renal transplant recipients, grafts infiltrated with more Tregs display much longer survival. Pediatric patients who acquired operational tolerance after liver transplantation showed increased levels of circulating Tregs compared with patients who received immunosuppression. Allograft tolerance in liver transplant recipients may be partly attributable to a higher frequency of circulating Tregs. Therefore, an increased level of circulating Tregs may be beneficial for allograft survival. Th17 cells are a subset of T helper cells which is characterized by the production of IL-17. Th17 cells have been suggested to play a role in allograft rejection in the context of organ transplantation. A study reported that cardiac allografts infiltrated with Th17 cells underwent accelerated vascular rejection in Tbet2/2 mice model. IL-17, a potent proinflammatory cytokine, has been demonstrated to participate in allograft rejection. It promotes cardiac allograft rejection by inducing the maturation, antigen presentation, and co-stimulatory capabilities of dendritic cells in mice. In a corneal transplant model, mice with deficient IL-17 experienced delayed graft rejection compared to wild-type mice. Blocking IL-17 promoted the maturation of dendritic cells, inhibited the proliferation of alloreactive T cells in vitro, and prolonged the survival time of vascularized cardiac allografts in vivo. IL-17 neutralization inhibits acute, but not chronic, vascular rejection in mice. Clinical evidence showed that the level of IL-17 in the blood is positively correlated with acute allograft rejection in the renal and the liver transplant recipients. Graft infiltrated with Th17 cells is associated with 
a faster destruction of allograft in renal transplant patients. The aforementioned evidence suggests that Tregs cells have a protective effect against graft rejection, whereas Th17 cells play an essential role in promoting graft rejection. The differentiation pathways of Tregs and Th17 cells are known to be antagonistic, and Tregs can be converted into Th17 cells under inflammatory conditions.