Research Article Polymorphic Variants of TNFR2 Gene in Schizophrenia and Its Interaction with -308G/A TNF-α Gene Polymorphism Renata Suchanek-Raif , 1,2 Pawel Raif , 3 Malgorzata Kowalczyk, 1,2 Monika Paul-Samojedny , 1,2 Krzysztof Kucia , 4,5 Wojciech Merk , 4,5 and Jan Kowalski 1,2 1 School of Pharmacy with the Division of Laboratory Medicine in Sosnowiec, Medical University of Silesia, Katowice, Poland 2 Department of Medical Genetics, Jedności 8 Street, 41-200 Sosnowiec, Poland 3 Department of Biosensors and Biomedical Signals Processing, Silesian University of Technology, Faculty of Biomedical Engineering, Roosevelta 40 Street, Zabrze, Poland 4 School of Medicine in Katowice, Medical University of Silesia, Katowice, Poland 5 Department of Psychiatry and Psychotherapy, Ziołowa 45 Street, 40-635 Katowice, Poland Correspondence should be addressed to Renata Suchanek-Raif; rsuchanek@sum.edu.pl Received 4 April 2018; Accepted 16 August 2018; Published 4 September 2018 Academic Editor: Sonja Pezelj-Ribarić Copyright © 2018 Renata Suchanek-Raif et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Aim. Many data showed a role of inflammation and dysfunction of immune system as important factors in the risk of schizophrenia. The TNFR2 receptor is a molecule that adapts to both areas. Tumor necrosis factor receptor 2 (TNFR2) is a receptor for the TNF-α cytokine which is a strong candidate gene for schizophrenia. The serum level of TNFR2 was significantly increased in schizophrenia and associated with more severe symptoms of schizophrenia. Methods. We examined the association of the three single nucleotide polymorphisms (rs3397, rs1061622, and rs1061624) in TNFR2 gene with a predisposition to and psychopathology of paranoid schizophrenia in Caucasian population. The psychopathology was measured by a five-factor model of the PANSS scale. We also assessed a haplotype analysis with the -308G/A of TNF-α gene. Results. Our case-control study (401 patients and 657 controls) revealed that the genetic variants of rs3397, rs1061622, and rs1061624 in the TNFR2 gene are associated with a higher risk of developing schizophrenia and more severe course in men. However, the genotypes with polymorphic allele for rs3397 SNP are protective for women. The rs1061624 SNP might modulate the appearance of the disease in relatives of people with schizophrenia. The CTGG haplotype build with tested SNPs of TNFR2 and SNP -308G/A of TNF-α has an association with a risk of schizophrenia in Caucasian population depending on sex. Our finding is especially true for the paranoid subtypes of schizophrenia. 1. Introduction The accurate pathogenesis of schizophrenia is still unknown. A deregulation of immune processes and inflammatory mechanisms in the central nervous system is suggested as important for the biology of schizophrenia. Evidence from the genetic, biomarker, and imaging studies strongly sup- ports the hypothesis. Cytokine abnormalities in particular are associated with the pathophysiology of schizophrenia [1]. TNF-α is one of the strongest candidates among proinflammatory cytokines. A significantly elevated level of TNF-α in the plasma of schizophrenia patients was found [2]. Its polymorphic variants, in particular -308G/A SNP, was associated with predisposition to schizophrenia [3]. TNF-α is an important modifier many of the processes in the CNS and plays a role in neurotransmission. It shows its activity through two receptors: TNFR1 and TNFR2 [4]. Both receptors are constitutively expressed by all neural cell types and have a region-specific reparative effect in brain, especially in the hippocampus and striatum [5, 6]. Those Hindawi Mediators of Inflammation Volume 2018, Article ID 8741249, 6 pages https://doi.org/10.1155/2018/8741249