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.
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http://dx.doi.org/10.1007/s00005-015-0360-z | DOI Listing |
Viruses
December 2024
Instituto René Rachou/Fiocruz Minas, Belo Horizonte 30190-009, MG, Brazil.
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 PDFPLoS One
January 2025
Neuroscience Center, King Fahad Specialist Hospital Dammam, Dammam, Saudi Arabia.
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 PDFImmunohorizons
January 2025
Division of Pulmonary Medicine, Department of Pediatrics, UPMC Children's Hospital of Pittsburgh, Pittsburgh, PA, United States.
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 PDFFront 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 PDFFEBS 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.
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