Contributions of type 17 immunity and type I interferon signaling to Salmonella-induced autoimmunity
type: CreativeWork
description: Autoimmune diseases can be broadly categorized into two groups: classical autoimmune disorders, such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), and post-infectious autoimmune conditions that arise as sequelae to microbial exposure. While several bacterial pathogens have been implicated in triggering such post-infectious autoimmunity, Salmonella is particularly well documented for its ability to induce an autoimmune-like condition known as reactive arthritis. While the mechanisms underlying infection-induced autoimmune sequelae remain unclear, type 17 and type I interferon (IFN) signaling play significant roles in the pathogenesis of many classical autoimmune diseases and bacterial infections. Previous research from our lab has shown that Salmonella biofilm-associated amyloid protein, curli, is a potent inducer of systemic inflammation and autoimmune responses. Curli induces immune responses via various receptors, on the cell surface through toll-like receptor (TLR) 2/1 and CD14, and in the cytosol through nucleotide-binding domain leucine-rich repeat family pyrin domain containing 3 (NLRP3). Curli and extracellular DNA (eDNA) form a strong bond that supports the structure of biofilms, resulting in a curli/DNA complex. This complex is recognized by TLR9 in the endosome. Through these receptors, curli induces inflammatory cytokines and chemokines, including interleukin (IL)-6, nitric oxide, IL-8, tumor necrosis factor (TNF)-α, IL-1β, IL-17, and type I IFN-related genes. In addition, systemic presence of curli is documented to induce autoimmune manifestations such as the generation of anti-double-stranded deoxyribonucleic acid (dsDNA) autoantibodies, anti-chromatin autoantibodies, and knee inflammation. Since prior work has demonstrated that curli can induce type 17 immunity and type I IFN signaling, we investigated the role of type 17 and type I IFN responses in Salmonella/curli-driven autoimmunity. We first investigated the role of type 17 i…
abstract: Autoimmune diseases can be broadly categorized into two groups: classical autoimmune disorders, such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), and post-infectious autoimmune conditions that arise as sequelae to microbial exposure. While several bacterial pathogens have been implicated in triggering such post-infectious autoimmunity, Salmonella is particularly well documented for its ability to induce an autoimmune-like condition known as reactive arthritis. While the mechanisms underlying infection-induced autoimmune sequelae remain unclear, type 17 and type I interferon (IFN) signaling play significant roles in the pathogenesis of many classical autoimmune diseases and bacterial infections. Previous research from our lab has shown that Salmonella biofilm-associated amyloid protein, curli, is a potent inducer of systemic inflammation and autoimmune responses. Curli induces immune responses via various receptors, on the cell surface through toll-like receptor (TLR) 2/1 and CD14, and in the cytosol through nucleotide-binding domain leucine-rich repeat family pyrin domain containing 3 (NLRP3). Curli and extracellular DNA (eDNA) form a strong bond that supports the structure of biofilms, resulting in a curli/DNA complex. This complex is recognized by TLR9 in the endosome. Through these receptors, curli induces inflammatory cytokines and chemokines, including interleukin (IL)-6, nitric oxide, IL-8, tumor necrosis factor (TNF)-α, IL-1β, IL-17, and type I IFN-related genes. In addition, systemic presence of curli is documented to induce autoimmune manifestations such as the generation of anti-double-stranded deoxyribonucleic acid (dsDNA) autoantibodies, anti-chromatin autoantibodies, and knee inflammation. Since prior work has demonstrated that curli can induce type 17 immunity and type I IFN signaling, we investigated the role of type 17 and type I IFN responses in Salmonella/curli-driven autoimmunity. We first investigated the role of type 17 i…
author: Bessho, Shingo
language: eng
keywords: Microbiology, Immunology, Medicine, Biomedical sciences
license: http://rightsstatements.org/vocab/InC/1.0/
date published: 2025-09
date modified: 2026-07-27T21:21:14Z
provider: Temple University
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: Temple University. Libraries