Background: sFasL is the soluble form of FasL inducing apoptosis by binding to Fas. Fas/sFasL could be the most important mechanisms in inflammatory conditions such as asthma by controlling inflammatory responses.This study was undertaken to determine the level of sFasL in allergic and non- allergic asthmatic patients with different stages of asthma control.Methods: Twenty asthmatic patients were enrolled and divided into controlled and uncontrolled patient groups.They were divided into 4 subgroups including controlled/allergic, controlled/non-allergic, uncontrolled/allergic and uncontrolled/non-allergic subgroups. Five normal subjects were selected as a control group. From all subjects, 3 ml of blood was obtained and sFasL and IgE serum levels were evaluated by a specific ELISA kit.Results: sFasL in the controlled and uncontrolled patient groups did not have any significant difference, but in the uncontrolled/allergic subgroup, it was significantly lower than that in the control group and also higher in the uncontrolled/non-allergic subgroup insignificantly.Conclusion: In patients with acute inflammatory conditions, sFasL had an increasing effect to control inflammation observed in uncontrolled/non-allergic subgroup, but unexpectedly not in the uncontrolled/allergic subgroup.Probably in allergic patients, there are factors or mechanisms that inhibit sFasL production or expression.

Background: Heart failure is the main cause of morbidity and mortality worldwide with poor prognosis. Two processes; inflammation and apoptosis, play major roles in the pathogenesis of heart failure with poor prognosis. Apoptosis can be discovered in different conditions within the myocardial tissues. One of the regulatory mechanisms of apoptosis is through Fas (CD95)/FasL system.Objective: Evaluating the level of soluble markers of Fas/FasL apoptosis system in patients with heart failure and its severity.Methods: This was a case-control study in which 85 patients with different functional class of heart failure and 25 healthy persons as control group were examined at Transplantation Institute of Moscow between the years 2004-2007. Evaluation of apoptosis markers was carried out by immunoferment analysis using an automatic analyzer (Personal Lab TM, Adaltis, Italy) and the Bender Med system kits, Austria.Findings: In patients with heart failure while the blood level of sFas was lower than that of healthy person, the sFasL was found to be higher compared to control group. Regarding the level of soluble forms of apoptotic markers of sFas/sFasL in HF, the sFas and sFasL levels were demonstrated to have an opposite association with the functional class of heart failure so that a negative relationship for sFas and a positive correlation for sFasL were found. At the same time, the sFas was shown to be weakly associated with ejection fraction whereas the sFasL demonstrated a reverse correlation (P<0.05). Conclusion: These markers could be used as complementary laboratory markers to assess the severity of heart failure and also the prognosis.

Background: Endometriosis is a common gynecological disorder, which its main feature is the growth of endometrial tissue outside the uterine cavity. In this disease, apoptosis is impaired in endometrial cells transmitted to the peritoneal cavity, and thus these cells remain in ectopic sites and grow there. FasL-expressing cells induce apoptosis when they bind to Fas-bearing immune cells. Soluble Fas ligand can be proteolytically cleaved from membrane-bound Fas ligand by metalloproteinases. Studies show that both soluble and membranous form of FasL in peritoneal cavity of endometriotic women can induce apoptosis of Fas bearing immune cells. Therefore, in this study the serum and peritoneal fluid levels of sFasL in patients with endometriosis compared with non-endometriotic subjects were evaluated. Methods: In this case-control study, which was performed from 2016 to 2017, peritoneal cavity of 19 patients with endometriosis and 19 healthy subjects, and also serum of 16 patients with endometriosis and 12 healthy subjects were studied. ELISA were used to determine the sFasL. Results: The results of this study showed that the amount of sFasL in peritoneal cavity of endometriosis patients is higher than healthy group, but this difference was not statistically significant (p=0. 07). Also, the serum sFasL level of patients was not different from control group. Conclusion: Expression of high sFasL in the peritoneal fluid can be one of the factors involved in the removal of Fas-expressing immune cells in the peritoneal fluid, which plays an essential role in the progression of the disease.

Background and Objectives: Apoptosis (programmed cell death) is an important regulatory event in spermatogenesis. Abnormally accelerated apoptosis in germ cells, may lead to an imbalance between cell proliferation and death, resulting in impairment in spermatogenic. Some studies have shown that glucocorticoids affect testialar homeostasis by decreasing of testosterone level. In the present study, the influence of dexametasone (Dex), a widely used glucocorticoid agent, on expression of FasL (FAS-Ligand) protein (a proapoptotic protein) in mouse testicular germ cells is investigated. Materials and Methods: Twenty-four adult male (6-8 weeks) mice were randomly divided into 3 groups. The first and second test groups received 2 and 7 mg/kg Dex per day, respectively, for 7 days. The control group received only saline daily for 7 days. One day after the final injection, the mice were sacrificed and the test groups were placed in formalin solution for immunohistochemistry studies. Positive immunoreactivity was calculated by H-score method. Results: The results revealed that expression of FasL in seminiferous epithelium is spermatogenic stage dependent, and the stage VII was the most susceptible to Dex. FasL expression was observed only at stages VII-VIII of spermatogenic cycle in 2 mg/kg Dex treated group (P<0.05). H-score was significantly increased in all stages of 7 mg/kg Dex treated group (P<0.05). The number of spermatocytes decreased significanhy in this group.Conclusions: It appears that glucocorticoid agents such as Dex, induces apoptosis by affecting proapoptotic proteins.