Abstract
The present study aimed to investigate the expression and association of the single-nucleotide polymorphism (SNP) -1637A/G in the promoter region of the T cell immunoglobulin domain and mucin domain protein-1 (Tim-1) gene in patients diagnosed with thymoma with or without myasthenia gravis (MG). The expression of Tim-1 was detected using the streptavidin peroxidase immunohistochemical staining method on tissues obtained from thymoma patients with (n=58) and without (n=62) MG. The Tim-1 gene -1637A/G polymorphism was detected using the single allele-specific primer polymerase chain reaction. The positive rate of Tim-1 expression in thymoma patients with MG was 62.1% (32/58), which was significantly higher compared with that in thymoma patients without MG (33.9%, 21/62) (P=0.002). The genotype frequencies of GG, GA and AA in the -1637A/G polymorphism were 0.7931, 0.2069 and 0, respectively, in thymoma patients with MG, and 0.6129, 0.3871 and 0, respectively, in thymoma patients without MG. A significant difference in the genotypes between the thymoma patients with MG and those without MG was found (P=0.031). In addition, a significant difference in allele frequencies between thymoma patients with MG and those without MG (P=0.024) was observed. The high expression of Tim-1 in thymoma tissues may play an important role in the development of thymoma with MG. The -1637A/G polymorphism site of the promoter region in Tim-1 may be associated with thymoma with MG. These findings provide a basis for further genetic research of thymoma with MG.
Highlights
Thymomas are primary tumors that arise from thymic epithelial cells (TEC) [1]
The present study aimed to investigate the expression of Tim‐1 in thymoma patients with and without myasthenia gravis (MG) and to examine whether the single‐nucleotide polymorphism (SNP) ‐1637A/G in the promoter region of the Tim‐1 gene contributes to the susceptibility of thymoma with MG
Capping experiments using human Jurkat T cells that expressed Tim‐1 suggest that Tim‐1 is associated with cluster of differentiation (CD) 3 and is recruited to the T cell receptor (TCR) signaling complex in human T cells [31]
Summary
Thymomas are primary tumors that arise from thymic epithelial cells (TEC) [1]. The thymus is a primary lymphoid organ that plays a role in regulating the proliferation and differentiation of T cells. The thymus typically starts to coalesce and becomes completely atrophic with remnant adipose tissue by the late teens, lymphopoiesis of the T cells continues during adult life [2]. Thymomas retain thymic cortical epithelial function to induce T‐cell differentiation [3]; they may lack normal mechanisms for selection of the T cell repertoire. Autoreactive T cells possibly emerging in a thymoma may trigger autoimmune disorders [4]. Thymomas are well‐known for their significant association with multiple autoimmune diseases, myasthenia gravis (MG). It has been reported that up to 50% of thymoma patients develop MG [5]
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