Assessment of interleukin 15 [il-15] gene polymorphism in adult patients with acute lymphoblastic leukemia

From its beginnings two decades ago with the analysis of chromosomal translocation break points, research into the molecular pathogenesis of acute lymphoblastic leukemia [ALL] has now progressed to the large scale sequencing of candidate genes that might be linked to the pathogenesis of leukemia. Interleukon-15 [IL-15] gene has gained the interest of many oncologist with five single nucleotide polymorphisms [SNPs] proved to be associated with childhood ALL. The aim of this study was to investigate the relationship between IL-15 gene polymorphisms and the risk for adult ALL and whether these polymorphisms are related to the immunophenotype of the disease. This study included 60 subjects classified into 2 groups: 30 patients with adult ALL [ALL group] and 30 healthy subjects of matched age and sex as control group. All subjects were genotyped for rs 10519613 and rs35964658 polymorphisms of IL-15 gene using PCR-RFLP technique.Results revealed that there was no statistical difference between ALL group and control group regarding the distribution of the genotypes of both for rs 10519613 and rs35964658 polymorphisms however there was 2.1 fold increased risk for ALL in C-allele carriers of rs 10519613 polymorphism [OR:2.1 95% CI: 0.45 - 9.84]. Concerning immunophenotype of the disease, there was no statistical difference between B-cell type and T-cell type regarding the distribution of the genotypes of the two polymorphisms, however there is 1.2 fold increased risk for B-cell type in G-allele carriers of rs35964658 polymorphism [OR: 1.2 95% CI: 0.07 - 19.63]. It wasconcluded that there was no association between both rs 10519613 and rs35964658 polymorphisms and neither the risk of ALL nor the immune-phenotype of the disease

Peritoneal fluid and serum concentrations of interleukine-6, interleukin-15 and tumor necrosis factor-alpha in women with endometriosis

The objective of this prospective controlled study was to investigate the ability of a group of serum and peritoneal fluid [PF] markers to predict non-surgical endometriosis. The study was conducted in Assiut University hospital, serum and PF samples were obtained from 40 women at the reproductive age, while undergoing laparoscopy for infertility or suspicious qf endometriosis. Concentrations of interleukin [IL] 6, IL-15 and tumor necrosis factor [TNF]-alpha were measured in serum and PF, by sandwich ELISA technique, and levels were compared among women who were allocated to groups according to post-surgical diagnosis, group I [endometriosis], included 24 patients, group II [non-endometriosis], included 7 women with peritoneal adhesions not related to endometriosis, and group III [control group], included 9 women without pelvic pathology. The endometriotic group was classified into 3 stages according to the revised American Fertility Society [I985] classification: Stage I, 11 patient, stage II, 8 patients and stage III, 5 patients. Results of this study revealed that serum IL-6 was significantly higher in endometriosis than in non-endometriosis and controls, serum TNF-alpha was significantly higher in endometriosis than controls with no significant difference with nonendometriosis. Serum IL- 15 was undetectable in all controls as well as about half of the endomoetriotic and non-endometriotic groups. As regards PF-IL-6, it showed no significant difference in comparing the 3 groups with each other. Both PF-TNF-alpha and PF-IL-15 were significantly higher in endometriosis than in non-endometriosis and controls and in non-endometriosis than controls. PF-IL- 15 levels were significantly higher in late stages of endometriosis and positively correlated with the stage of endometriosis. In conclusion only serum IL-6, PF-IL-15 and PF-TNF-alpha could be used to discriminate between patients with and without endometriosis. Before these markers can be used as a non-surgical diagnostic tool, these data should be verified in a larger study PF-IL-15 is the only marker that is affected by the stage of endometriosis and so, it can be used us a quantitative rest for severity of the disease

Complicated malaria is associated with differential elevations in serum levels of interleukins 10, 12, and 15.

Complicated malaria, caused by Plasmodium falciparum, is characterized by multiple organ dysfunction. The pathogenesis of complicated malaria involves complex host-parasite interactions that include polarized cytokine responses. Recently, correlates between Th1-like and Th2-like cytokines, especially interleukin-10 (IL), IL-12, and TNF-alpha, and specific types of organ dysfunction have been noted. Here, we measured IL-10, IL-12, and for the first time, IL-15, in 19 patients aged 16-55 years old with complicated malaria on days 0 (admission), 3, 7, and 14. For analysis, patients were grouped together or sub-categorized into hyperparasitemias or cerebral malaria (CM). For IL-10, a dramatic increase was noted on admission, followed by a reduction toward control values that closely paralleled parasite clearance. For IL-12, modest but persistent increases were noted over the entire 14 day period that did not correlate with parasitemia. In general, especially on days 0 and 3, hyperparasitemic patients had, in comparison with CM patients, higher IL-10 and IL-12 levels. In contrast, IL-15 was generally below detection in most samples. These results provide further insight into the pathogenesis of complicated malaria by strengthening the contention that cytokines such as IL-10 and IL-12 are involved in modulating the immune response to P. falciparum.

Elevated serum interleukin-15 levels in systemic lupus erythematosus

Interleukin-15 (IL-15) has multiple biological properties, including the induction of other cytokine production and the inhibition of T cell apoptosis. Recently, IL-15 was reported to have a major role in synovial inflammation of rheumatoid arthritis, and that it provokes and amplifies the inflammatory process through the activation of TNF-alpha production. In systemic lupus erythematosus (SLE), the dysregulation of apoptosis and various cytokine production were observed and have been implicated in the pathogenesis of SLE. Thus, we tried to determine serum IL-15 levels in SLE patients and to assess the relationship among IL-15 levels, TNF-alpha levels and disease activity of SLE. Twenty SLE patients and 10 controls were studied. Paired serum samples were collected from all SLE patients at the time of presentation with active disease and at 4 weeks after institution of treatment. IL-15 levels were determined by ELISA and compared with the disease activity indices in SLE. The disease activity of SLE was measured using the SLE Disease Activity Index (SLEDAI) and laboratory parameters such as circulating immune complex (CIC), C3, C4, anti-DNA antibody, IgG, IgM, and IgA. The IL-15 levels in SLE patients were significantly higher than those of controls (5.38 +/- 4.89 vs. 1.04 +/- 1.26 pg/ml). However, elevated IL-15 levels did not correlate with the SLEDAI, nor did they correlate with other laboratory activity indices. The changes in serum IL-15 levels did not correlate with the changes in serum TNF-alpha in the disease course of SLE patients, whereas TNF-alpha reflected the changes in disease activity of SLE. Serum levels of IL-15 are elevated in SLE patients, but IL-15 did not correlate with the disease activity of SLE. TNF-alpha production in SLE patients was unlikely to be related with IL-15.