Cutaneous leishmaniasis (CL) is caused by different species of the genus Leishmania. Pro- and anti-inflammatory cytokines play different roles in resistance/susceptibility and the immunopathogenesis of Leishmania infection. The balance and dynamic changes in cytokines may control or predict clinical outcome. T helper 1 (Th1) inflammatory cytokines (especially interferon-γ, tumor necrosis factor-α and interleukin-12) are the crucial factors in the initiation of protective immunity against L. major infection, whereas T helper 2 cytokines including IL-5, IL-4, and IL-13 facilitate the persistence of parasites by downregulating the Th1 immune response. On the other hand, aggravation of inflammatory reactions leads to collateral tissue damage and formation of ulcer. For this reason, immunity system such as T regulatory cells produce regulatory cytokines such as transforming growth factor-β and IL-10 to inhibit possible injures caused by increased inflammatory responses in infection site. In this article, we review the role of pro- and anti-inflammatory cytokines in the immunoprotection and immunopathology of CL.

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SUMMARYPrevious studies have shown that Leishmania elongation initiation factor (LeIF) antigen causes a partial immunity against leishmaniasis. The antigen develops type I immunity by overexpression of inflammatory cytokines such as interleukin-12 (IL-12), IFN-c and TNF-a. Therefore, We evaluated immune responses induced by the LeIF gene against Leishmania major infection. Immunization with LeIF gene alone or with IL-12 induced Th1 response and produced higher IFN-c and lower IL-4 levels by splenocytes than control groups (P < 0Á05) and also ratios of IFN-c/IL-4 were 11Á68 to 18Á53 times more in immunized groups than control groups after challenge. In addition, analysis of humoral immune response revealed that immunized mice had more IgG2a levels than both control groups (P < 0Á05). On the other hand, lesion size was less for immunized animals than control groups from 4th week after challenge (P < 0Á05). The percentage reduction in lesion size was 29Á30% for LeIF and 51Á98% for LeIF + IL-12 than PBS at 12th week postinfection. Spleen parasite burden decreased in all immunized groups in comparison with control groups (P < 0Á05). The results indicated that LeIF gene induced partial immunity against L. major infection in BALB/c mice. However, LeIF plus IL-12 group showed more potent immunity with smaller lesions than other groups.

Visceral leishmaniasis is an important neglected parasitic disease that is generally caused byLeishmania infantum,Leishmania donovaniandLeishmania chagasi. However, several causative species of cutaneous leishmaniasis (CL) causes an interstitial form of leishmaniasis which known viscerotropic leishmaniasis. The aim of this paper is a systematic review of the cases of viscerotropic leishmaniasis to present the main causative agents, clinical manifestations, treatment and outcomes of the cases. An electronic search (any date to August 2017) without language restrictions was performed using Medline, PubMed, Scopus and Google Scholar. The searches identified 19 articles with total 30 case reports. Of them, old worldLeishmaniaspecies was reported from 23 (76.7%) cases, including 20 cases ofL. tropicaand three cases ofL. major; whereas new worldLeishmaniaspecies were reported in seven (23.4%) cases. The infection was more prevalent in male (24/30, 80%) than female (5/30, 16.7%) patients. Co-morbidity/co-infection was observed in 13 out of 30 cases (43.4%), which the most of them was HIV/AIDS (10 out of 13 cases, 76.9%). The results suggested that viscerotropic leishmaniasis should be more attended in the endemic countries of CL and in immunocompromised patients in order to exact discrimination from other endemic infectious diseases.

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