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  • The immunohistochemistry showed infiltration of


    The immunohistochemistry showed infiltration of CD3+ T cells in dermis and few in the epidermis. The double staining of vitiligo biopsies by CD3+ and CD4+ showed that most of CD3+ cells are also CD4+. Whereas, CD3+/CD8+ are present in leading edge and lesional vitiligo skin and showing a mixture of CD8+ and CD4+ T cells beside the appearance of Th17 and Th1. However, double staining by CD3+ and FoxP3+ showed a significantly reduced percentage of Tregs among infiltrating T cells in non-lesional, perilesional and lesional vitiligo skin compared to normal skin from healthy adults [28]. In vitiligo perilesional skin, the increase in CD8+ T cells was not accompanied by increase in Tregs (called Tregs pausing). This significant reduction in Tregs is associated with marked reduction in CCL22 expression by 43% in vitiligo lesions comparing to controls, whereas the mode of expression of CCL17 and CCL1 was normal which lead to suggestion that a reduction in CCL22 expression is primarily responsible for impaired homing of Tregs. Whereas functional Tregs are abundant in the circulation [18]. So this support the hypothesis looking at autoimmune diseases as an increase in CTL comparing to Tregs and failure of Tregs to control CTL so as to keep “peripheral tolerance”.
    Diabetes type 1 Auto-reactive T cells against insulin-producing pancreatic langerhans-islet are known in diabetes type-I. They are blocked by ARCA [29] or transferred Tregs [30]and showed good result in cessation of the progressive beta-cell damage. Montane. J et al., 2011 prevented marine auto-immune diabetes by intra-pancreatic duct injection of double stranded adeno-associated virus encoding CCL22 [31]. This resulted in increase of CCL22 level in the pancreatic islet and recruited endogenous regulatory T cells. The result of this experiment was challenging because it resulted in prevention of β cells destruction by auto-reactive T cells, sustained the protection against auto-immune diabetes in NOD mice and delayed the relapse of diabetes. Added to that, it increased the frequency of TGF- β producing CD4+ regulatory T cells around the pancreatic islet and decreased the frequency of circulating CD8+, IFN- γ producing autoreactive T cells.
    Bioinspired controlled release of CCL22 Siddharth Jhunjhunwala et al. (2012) designed a control released vehicle for CCL22 and tested their device in many mice models. The device was effectively able to delay rejection of allogenic cells transferred to the site previously injected by CCL22MP. They found excessive migration of regulatory T cells to the site of injection in response to CCL22 controlled release [32]. They finally concluded that the site-specific attraction of Tregs leading to local immunomodulation can be achieved in vivo using CCL22MP.
    Conflict of interest
    Introduction Dendritic cells (DC)-based immune-therapy (commonly called “therapeutic vaccine”) has been reported as an interesting approach to induce a control of plasma viral load (PVL) in HIV positive (HIV+) patients as well as an important tool for deeper investigating the correlation of protection against HIV infection in these patients. Since the first published results [1–3], it appeared that not all the immunized patients uniformly respond to the treatment, opening a plethora of question about the characterization of factors that might affect the out-come of immunization, and the definition of guide lines to appropriately choose individuals with greatest chance to effectively respond to immune-therapy. Genetics screening of HIV+ patients submitted to the first-phase clinical ARCA trial of a French-Brazilian DC-based vaccine [3] evidenced that polymorphisms in MBL2, NOS1, PARD3B and CNOT1 genes were associated with a weak or transient response (not significantly diminished PVL) observed in half of 18 treated subjects [4–6]. The profile of “weak/transient” or “good” responder may also depend on several factors, other than host genome, such as the quality of DC obtained in vitro from patient\'s peripheral blood monocytes, and the ability of patient\'s immune system to be activated by the in vitro manipulated DC. Considering that immune response of HIV+ individuals is greatly impaired by HIV-1 infection itself, questions about the responsiveness to a DC-based vaccine are strictly correlated with the ability of each individual to counteract the infection.