Serovar Typhimurium Travels to Mesenteric Lymph Nodes Both with Host Cells and Autonomously.

infection is a globally important cause of gastroenteritis and systemic disease and is a useful tool to study immune responses in the intestine. Although mechanisms leading to immune responses against have been extensively studied, questions remain about how bacteria travel from the intestinal mucosa to the mesenteric lymph nodes (MLN), a key site for Ag presentation. In this study, we used a mouse model of infection with serovar Typhimurium (STM) to identify changes in intestinal immune cells induced during early infection.

Role of Gut Inflammation in Altering the Monocyte Compartment and Its Osteoclastogenic Potential in HLA-B27-Transgenic Rats.

Objective: To investigate the relationship between intestinal inflammation and the central and peripheral innate immune system in the pathogenesis of HLA-B27-associated spondyloarthritis using an HLA-B27-transgenic (B27-Tg) rat model.

Methods: The myeloid compartment of the blood and bone marrow (BM) of B27-Tg rats, as well as HLA-B7-Tg and non-Tg rats as controls, was evaluated by flow cytometry. Plasma from rats was assessed by enzyme-linked immunosorbent assay for levels of CCL2 and interleukin-1α (IL-1α).

Dendritic cells and regulatory T cells in spondyloarthritis.

Purpose Of Review: The spondyloarthropathies (SpAs) are a group of interrelated inflammatory disorders with overlapping clinical features. Current SpA treatments only provide partial symptomatic and functional relief in a subgroup of patients. Consequently, there is a need to better understand the pathophysiology of SpA to develop more specific and effective treatments for these conditions.

Expression of aberrant HLA-B27 molecules is dependent on B27 dosage and peptide supply.

Objectives: Cellular expression of non-classical forms of human leukocyte antigen (HLA)-B27 (NC-B27) may be involved in spondyloarthritis (SpA) pathogenesis. We used a novel B27-specific monoclonal antibody, HD6, to ask if B27 transgenic (TG) rat splenocytes express these NC-B27 molecules. We also investigated whether B27-binding peptides could affect the expression and functional immune recognition of HD6-reactive B27 molecules.

Expression of HLA-B27 causes loss of migratory dendritic cells in a rat model of spondylarthritis.

Objective: In rats transgenic for human HLA-B27 and β(2) -microglobulin (B27-transgenic rats), colitis and peripheral inflammation develop spontaneously. Therefore, B27-transgenic rats provide a model of spondylarthritis. Because inflammation in these rats requires CD4+ T lymphocytes and involves intestinal pathology, we hypothesized that dendritic cells (DCs) that migrate from the intestine and control CD4+ T cell differentiation would be aberrant in B27-transgenic rats.