Tolouei et al. : IL-23 and IL-27 Levels in Macrophages Collected … Fig. 3: Cytokine production from Macrophages in patients’ with healing and non healing lesions. Macro- phages were stimulated with or without live L. major promastigotes. After 24hours supernatants were as- sayed for IL-27 production. Results were obtained by an ELISA assay .Difference between cytokine pro- duction in stimulated and unstimulated macrophages in healing group (a), difference between cytokine production in stimulated and unstimulated macrophages in non- healing group(b)and difference between a and b(c). Data are expressed as the mean ± standard deviation of the mean. Significant differences were shown between these groups (P < 0.001) Discussion Although immune responses in leishmaniasis have been studied but still no surrogate mark- er(s) of healing and protection in human is identified (8-12). IL-12, IL-23 and IL-27 are related to the family which stimulates Th1 type of immune response. Effective immune re- sponse in intracellular parasites such as Trypanosoma cruzi, Toxoplasma gondii and Leishmania major is Th1 type of response (11, 26). In this study the level of IL-23 and IL-27 were studied to explore possible relationship between IL-23 and IL-27 and healing process in patients with CL caused by L. major. The results showed that the level of IL-23 and IL-27 in both groups of patient were elevated after the macrophages were stimulated with L. major. Moreover, the difference of IL- 23 and IL- 27 levels before and after stimulation was signifi- cantly (P<0.001) different between macrophag- es collected from patients with healing and non- healing form of the lesion. The differences was seen in IL-23 and IL-27 production in these two Available at: http://ijpa.tums.ac.ir groups might be due to different interaction be- tween the structures referred to pathogen-asso- ciated molecular patterns (PAMPs) that are recognized by pathogen recognition receptors (PRRs) of innate immune system (27). Another possibility is that different intracellular signal- ing pathway or adaptor molecules might be in- volved (28). This alteration may result from a difference in regulatory factors, enhancers and inhibitor molecules due to primary expression of cytokines (29). In the past few years immune responses against Leishmania infection and cy- tokine profile in human and animal leishma- niasis have been deeply studied (7, 8, 10, 11, 30). It is reported that IL-27 showed in vitro capacity to inhibit Th2 cell differentiation (31) and in another study it is shown that daily in vivo treatment of Leishmania major infected BALB/c mice by IL-27 induced lower parasite burden via up regulation of Th1 responses (22). It also shown that although IL-27 and its recep- tor are promoters of Th1 differentiation, but 23