Infectious agents are plausible environmental triggers for autoimmunity in genetically susceptible individuals. Polymorphic variants of genes implicated in innate immunity may affect immune responses and hence promote auto-aggressive reactions. Genes such as Toll-like receptor-3 (TLR3), which participate in recognizing conserved foreign molecules and mounting the first line of defence against viral infections, are promising functional candidates in autoimmune conditions. We investigated the association of the TLR3 variants, rs13126816 and rs3775291, with the autoimmune endocrine disorders, Addison's disease (AD) and type 1 diabetes (T1D) in the Polish population. The study comprised 168 AD patients, 524 individuals with T1D and 592 healthy controls. Genotyping was performed by real-time PCR. Distribution of the TLR3 genotypes and alleles did not reveal significant differences between patients and controls (p > 0.05). No effect on age at disease onset was found in affected cohorts. This analysis does not support an association between TLR3 variants and the risk for autoimmune destruction of the adrenal cortex and beta cells. However, innate immunity merits further studies in autoimmune endocrine conditions.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4713709PMC
http://dx.doi.org/10.1007/s00005-015-0360-zDOI Listing

Publication Analysis

Top Keywords

toll-like receptor-3
8
type diabetes
8
innate immunity
8
association tlr3
8
tlr3 variants
8
autoimmune endocrine
8
autoimmune
5
polymorphisms toll-like
4
receptor-3 gene
4
gene autoimmune
4

Similar Publications

The global number of COVID-19 deaths has reached 7 million, with 4% of these deaths occurring in children and adolescents. In Brazil, around 1500 children up to 11 years old died from the disease. The most common symptoms in children are respiratory, potentially progressing to severe illnesses, such as severe acute respiratory syndrome (SARS) and MIS-C.

View Article and Find Full Text PDF

Hepatitis C Virus (HCV) is a blood borne pathogen that affects around 200 million individuals worldwide. Immunizations against the Hepatitis C Virus are intended to enhance T-cell responses and have been identified as a crucial component of successful antiviral therapy. Nevertheless, attempts to mediate clinically relevant anti-HCV activity in people have mainly failed, despite the vaccines present satisfactory progress.

View Article and Find Full Text PDF

Influenza virus infects millions each year, contributing greatly to human morbidity and mortality. Upon viral infection, pathogen-associated molecular patterns activate pattern recognition receptors on host cells, triggering an immune response. The CD209 protein family, homologs of DC-SIGN (dendritic cell-specific intercellular adhesion molecule 3-grabbing nonintegrin), is thought to modulate immune responses to viruses.

View Article and Find Full Text PDF

Interleukin-32 positive immune and resident cells in kidney samples from lupus patients: a pilot study.

Front Immunol

January 2025

Rheumatology Unit, Department of Clinical Internal, Anesthesiologic and Cardiovascular Sciences, "Sapienza" University of Rome, Rome, Italy.

Introduction: Lupus nephritis (LN), caused by immune complexes produced or deposited from the bloodstream, is one of the most severe features of Systemic Lupus Erythematosus (SLE) leading to an increased morbidity and mortality. Toll like receptors (TLRs), such as TLR3, TLR7 and TLR9, may play a key role in its pathogenesis. Interleukin-32 (IL-32), a cytokine involved in both innate and adaptive immune responses, has been widely considered in autoimmune-inflammatory rheumatic diseases.

View Article and Find Full Text PDF

TNFAIP3-interacting protein 1 (ABIN-1) negatively regulates caspase-8/FADD-dependent pyroptosis.

FEBS J

January 2025

Department of Biochemistry and Molecular Biology, School of Medicine, Southeast University, Nanjing, China.

TNFAIP3-interacting protein 1 (TNIP1; also known as ABIN-1) is a ubiquitin-binding protein that suppresses death-receptor- or Toll-like receptor-mediated apoptosis and necroptosis; however, it remains unclear whether ABIN-1 is capable of regulating pyroptosis. In the present study, we found that, in mouse embryonic fibroblasts and macrophages, ABIN-1 deficiency sensitized cells to poly(I:C) + TAK1 inhibitor 5Z-7-oxozeaenol-induced pyroptosis besides apoptosis and necroptosis. The sensitizing effect of ABIN-1 deficiency on pyroptosis depended on caspase-8 and its adaptor molecule FAS-associated death domain protein.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!