Polymorphisms in the TGFB1 and FOXP3 genes are associated with the presence of antinuclear antibodies in chronic hepatitis C

被引:0
|
作者
Costa de Castro, Geison Luiz [1 ]
Bichara, Carlos David A. [1 ]
Santiago, Angelica Menezes [1 ]
de Brito, William Botelho [1 ]
Soares Pereira, Leonn Mendes [1 ]
Ferreira Moura, Tuane Carolina [1 ]
Graca Amoras, Ednelza da Silva [1 ]
Moura de Araujo, Mauro Sergio [1 ,2 ]
Souza da Silva Conde, Simone Regina [2 ]
Freitas Queiroz, Maria Alice [1 ]
Ishak, Ricardo [1 ]
Rosario Vallinoto, Antonio Carlos [1 ]
机构
[1] Univ Fed Para, Inst Ciencias Biol, Lab Virol, Belem, Para, Brazil
[2] Univ Fed Para, Hosp Univ Joao de Barros Barreto, Belem, Para, Brazil
关键词
Microbiology; Immunology; Virology; Immune response; Viruses; Infectious disease; Chronic hepatitis C; Ana; TGF-beta; 1; FOXP3; Polymorphisms; GROWTH-FACTOR-BETA; T-CELLS; AUTOANTIBODIES; TGF-BETA-1; INHIBITION; EXPRESSION; MECHANISM; TYPE-1; LIVER;
D O I
10.1016/j.heliyon.2020.e04524
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Chronic infection with Hepacivirus C (HCV) can lead to the occurrence of antinuclear antibodies (ANAs) and changes in cytokine profiles that can be similar to autoimmune diseases. The aim of the study was to identify polymorphisms in important mediators of the immune response in association with ANAs, which could contribute to the development of autoimmunity in hepatitis C. The study included 87 patients with chronic hepatitis C who were evaluated for the presence of ANA (indirect immunofluorescence) and for polymorphisms in the FOXP3, IFNG, IL6, IL8, IL10, MBL2, CRP, TGFB1 and TNFA genes (real-time PCR). Of the patients evaluated, 17 (19.54%) had ANA reactivity. The G allele of the FOXP3 rs2232365 polymorphism was more frequent in ANA-positive women (p = 0.0231; OR = 3,285). The C allele of the TGFB1 rs1800469 polymorphism was associated with ANA production (p = 0.0169; OR = 2.88). The results suggest that polymorphisms in genes related to immunological regulation may be associated with mechanisms that lead to the emergence of autoantibodies in the context of chronic Hepacivirus C infection.
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