Abstract
Toll-like receptors (TLRs) are important initiators of the immune response, both innate and acquired. Evidence suggests that gene polymorphisms within TLRs cause malfunctions of certain key TLR-related signaling pathways, which subsequently increases the risk of autoimmune diseases. We illustrate and discuss the current findings on the role of Toll-like receptor gene polymorphisms in numerous autoimmune diseases in this review, such as type 1 diabetes mellitus, Graves’ disease, rheumatoid arthritis, systemic lupus erythematosus and multiple sclerosis. The study of genetic variation in TLRs in different populations has shown a complex interaction between immunity and environmental factors. This interaction suggests that TLR polymorphisms affect the susceptibility to autoimmune diseases differently in various populations. The identification of Toll-like receptor gene polymorphisms can expand our understanding of the pathogenesis of autoimmune diseases, which will subsequently guide effective medical management and provide insight into prognosis and advanced treatments.
Highlights
Autoimmune diseases develop when the immune response is misdirected to the host [1]
Some Toll-like receptors (TLRs) gene polymorphisms may be the result of positive selection, and such polymorphisms may have protective or deleterious effects against infections caused by certain pathogens, and affect the development of autoimmune diseases
Numerous studies have highlighted the important role of TLRs in autoimmune diseases
Summary
Autoimmune diseases develop when the immune response is misdirected to the host [1]. These diseases range from organ-specific diseases (in specific tissues, antibodies and T cells react to selfantigens) to organ-nonspecific or systemic diseases (characterized by reactions to antigens distributed in multiple tissues) [2]. In 2005, similar studies were conducted in South African T1DM patients to determine the association between this disease and possible polymorphisms of genes in TLR3. These studies, which recognized three SNPs (rs5743313 [2593 C/T], 2590 G/C, and rs5743315 [2642 C/A]) presented ambiguous results [7, 59]. The data on GD suggest that patients with identified TLR gene polymorphisms have disease susceptibility, they are not sufficient to thoroughly assess the molecular mechanisms underlying the aforementioned susceptibility Most of these studies were conducted using small sample sizes involving individuals from a single ethnic group, which significantly reduces the reliability of the results obtained regarding the risk of disease development. There are no studies on the development of SNPs and MS for the NF-kB gene; further investigations are warranted
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