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Behçet’s disease (BD) is a systemic, autoinflammatory, chronic disorder which affects various parts of the body in genetically susceptible individuals. BD has a multi-factorial etiopathogenesis which encompasses both innate and adaptive arms of immunity. NK cells, which kill virus-infected or malign cells and provide interaction between adaptive and innate immune system, are also known to involve in the pathogenesis of autoimmune/autoinflammatory diseases including BD. NK cells function in immune responses via the signals obtained from surface-expressed activating and inhibitory receptors. In this study, we aimed to explore NK cell activation status by measuring the levels of activation marker CD69 and activating receptors NKG2D, NKp30, and NKp46 as well as proliferative and cytotoxic capacities in response to stimulation with interleukin (IL)-15-combined cytokines in BD patients. CD4+ and CD8+ T cell responses were also evaluated to compare with those of NK cells. As a result, the expression of activating receptors on NK cells was demonstrated to be varied among patients with active and inactive BD and healthy controls. The proliferation levels of NK cells were elevated in BD patients, especially in inactive phase of disease compared to healthy controls. Additionally, CD107a levels of inactive BD patients were detected to be lower in comparison with healthy controls and active BD patients. These findings suggest that BD patients in active and inactive phases display different activation status of NK cells which indicate NK cells might be associated with immune attacks and remissions during the course of BD.

The two polymorphisms [IL-12 (-1188) A/C and the IFN-γ (+874) A/T)] are known to have functional consequences and henceforth were analyzed in subacute sclerosing panencephalitis (SSPE) patients to reveal a possible relation with these polymorphisms and this debilitating disease. For the IL-12 (-1188) A/C polymorphism, 78 patients and 90 healthy individuals were analyzed. An increase in the AA genotype was determined ( p  = 0.02, OR = 2.06). There was also a statistically significant difference between the control group and the patients with respect to the allele frequencies ( p  = 0.04, OR = 1.65). For the IFN-γ (+874) A/T polymorphism, 69 SSPE patients and 115 controls were studied and there was not a significant difference between the two groups. Our findings suggested that not the IFN-γ (+874) A/T but the IL-12 (-1188) A/C polymorphism is correlated with SSPE and having an AA genotype or A allele decreases the risk of developing SSPE by 2.06- and 1.65-fold, respectively.

Objective: Pemphigus, expressing a life-threatening blistering disease, result from autoantibodies against the proteins that mediate intercellular adhesion in desmosomes, namely desmoglein 1 and/or 3. The importance of cytotoxic T lymphocyte-associated antigen (CTLA)-4 in negative regulation of T lymphocytes, which take part in this autoimmune reaction, is well known. Gene polymorphisms regarding this molecule affect autoimmunity. We aimed to determine whether CTLA-4 +49 A/G, -318 C/T, -1661 A/G and CT60 A/G gene polymorphisms cause susceptibility to pemphigus in Turkish population. Methods: We detected genotypes of the single nucleotide polymorphisms for 118 pemphigus patients and 108 healthy individuals with the help of polymerase chain reaction-restriction fragment length polymorphism method. Results: Distribution of the CTLA-4 +49 A/G, -318 C/T, -1661 A/G and CT60 A/G allele and genotype frequencies did not differ between pemphigus patients and healthy controls (p=0.643, OR=0.931; p=0.847, OR=1.160; p=0.968, OR=0.975; p=0.173, OR=1.303, respectively). Conclusion: We concluded that these polymorphisms are not associated with pemphigus susceptibility in Turkish population. This is the first study investigating the possible role of the 4 CTLA single nucleotide polymorphism in pemphigus susceptibility simultaneously. The role of CTLA-4 -1661 A/G gene polymorphism in pemphigus was not studied previously.