Abstract
Controversial observations have been published on the association of the cytotoxic T lymphocyte associated antigen gene's variants with rheumatoid arthritis (RA). After genotyping 428 patients and 230 matched controls, the prevalence of the CT60∗G allele was more frequent in RF- and/or anti-CCP-seropositive RApatients, compared to the healthy controls (P < .001). Regression analysis revealed that the CT60∗G allele is a possible predisposing factor for RA in these subgroups. No accumulation of the +49∗G allele was found among patients, and this variant was not found to correlate with RA. Assaying the possible genotype variations, the +49∗G-C T60∗G allelic combination was accumulated in seropositive RA-subtypes, and was associated with the risk of RA (OR = 1.73, P = .001 for the whole RA-population). Although the +49∗G allele did not mean a predisposition to RA alone, in combination with C T60∗G it, also conferred risk, suggesting that the +49A/G variant is associated with the risk of RA only in certain haplotypes.
Highlights
The cytotoxic T lymphocyte associated antigen (CTLA4) is a well-known cosignalling molecule of the B7 receptor immunoglobulin family
Contrary to CD28, which transmits a stimulatory signal to the T cells by binding to B7-1 or B7-2 receptors on antigen presenting cells, CTLA4 is an inhibitory factor in T-cell activating systems [1]
The CTLA4 gene polymorphisms are reportedly associated with a variety of T cell-mediated autoimmune diseases such as type 1 diabetes mellitus [2, 3], systemic lupus erythematosus, Hashimoto thyroiditis [4], Addison disease [5], Grave’s disease [6,7,8], multiple sclerosis [9,10,11], and celiac disease [12, 13]
Summary
The cytotoxic T lymphocyte associated antigen (CTLA4) is a well-known cosignalling molecule of the B7 receptor immunoglobulin family. CTLA4 is expressed by CD4+, CD8+, T and B lymphocytes, and is located on the surface of the cell. Its expression and its density on the cell surface is affected by the activation of the T lymphocytes. Contrary to CD28, which transmits a stimulatory signal to the T cells by binding to B7-1 or B7-2 receptors on antigen presenting cells, CTLA4 is an inhibitory factor in T-cell activating systems [1]. The CTLA4 gene polymorphisms are reportedly associated with a variety of T cell-mediated autoimmune diseases such as type 1 diabetes mellitus [2, 3], systemic lupus erythematosus, Hashimoto thyroiditis [4], Addison disease [5], Grave’s disease [6,7,8], multiple sclerosis [9,10,11], and celiac disease [12, 13]. Previous investigations on the association of CTLA4 with RA [14,15,16,17,18,19,20,21,22] resulted in controversial outcomes
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