Division of Infectious Disease, Department of Medicine, Vanderbilt University School of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Published: January 2024
AI Article Synopsis
Article Abstract
Activation of Th17 cell responses, including the production of IL-17A and IL-21, contributes to host defense and inflammatory responses by coordinating adaptive and innate immune responses. IL-17A and IL-17F signal through a multimeric receptor, which includes the IL-17 receptor A (IL-17RA) subunit and the IL-17RC subunit. IL-17RA is expressed by many cell types, and data from previous studies suggest that loss of IL-17 receptor is required to limit immunopathology in the model of infection. Here, an mouse was generated on the FVB/n background, and the role of IL-17 signaling in the maintenance of barrier responses to was investigated. Generating the on the FVB/n background allowed for the examination of responses in the paragastric lymph node and will allow for future investigation into carcinogenesis. While uninfected mice do not develop spontaneous gastritis following infection, mice develop severe gastric inflammation accompanied by lymphoid follicle production and exacerbated production of Th17 cytokines. Increased inflammation in the tissue, increased IgA levels in the lumen, and reduced production of Muc5ac in the corpus correlate with increased induced paragastric lymph node activation. These data suggest that the cross talk between immune cells and epithelial cells regulates mucin production, IgA production, and translocation, impacting the integrity of the gastric mucosa and therefore activating of the adaptive immune response.
Pathobionts have evolved many strategies to coexist with the host, but how immune evasion mechanisms contribute to the difficulty of developing vaccines against pathobionts is unclear. Meanwhile, Staphylococcus aureus (SA) has resisted human vaccine development to date. Here we show that prior SA exposure induces non-protective CD4 T cell imprints, leading to the blunting of protective IsdB vaccine responses.
Retinoid-related orphan receptor-γ (RORγ) is a nuclear receptor that plays important roles in the development and activation of T helper type-17 (Th17) cells. In this study, we characterized the pharmacological profile of JTE-151 ((4S)-6-[(2-chloro-4-methylphenyl)amino]-4-{4-cyclopropyl-5-[cis-3-(2,2-dimethylpropyl)cyclobutyl]isoxazol-3yl}-6-oxohexanoic acid), which is a novel RORγ antagonist identified by our group. JTE-151 dissociated co-activator peptide from the human RORγ-ligand binding domain (LBD) and recruited co-repressor peptide into human RORγ-LBD, and potently inhibited the transcriptional activity of RORγ of human, mouse and rat.
γδ T cells play diverse roles in immune responses, producing either IL-17A or IFN-γ. Here we investigated the impact of this functional dichotomy on cutaneous leishmaniasis. We demonstrate that in Sv129 mice susceptible to Leishmania amazonensis, Vγ4+ γδ T cells are the main source of IL-17A.
Background: Acute Respiratory Distress Syndrome (ARDS) is a severe lung condition posing significant health risks. Observational studies have indicated a potential linkage between ARDS and various interleukins, such as Interleukin-8, -2, -6, and -1β. However, the causal relationships between specific interleukins, their receptors, and ARDS remain unclear.
Department of Dermatology, University of Minnesota, Minneapolis, Minnesota; Department of Medicine, University of Minnesota, Minneapolis, Minnesota; Departments of Medicine and Dermatology, Minneapolis VA Health Care System, Minneapolis, Minnesota. Electronic address:
Hidradenitis suppurativa (HS) is an autoinflammatory condition characterized by abscesses, inflammatory nodules, and tunnels in intertriginous sites of the body. The pathogenesis of HS involves follicular occlusion in combination with environmental, genetic, hormonal, and metabolic factors. HS lesions are characterized by an influx of neutrophils, histiocytes, B and T cells, and upregulation of proinflammatory cytokines such as tumor necrosis factor-α, interleukin-1, interleukin-17, and interferons.
