Brucella canis is a small intracellular Gram-negative bacterium that frequently leads to chronic infections highly resistant to antibiotic therapy in dogs. Also, it causes mild human brucellosis compared to other zoonotic Brucella spp. Herein we characterize the cellular immune response elicited by B. canis by analysing human and canine CD4 T cells after stimulation with autologous monocyte-derived dendritic cells (MoDCs). Human and canine B. canis-primed MoDCs stimulated autologous CD4 T cells; however, a Th1 response was triggered by human MoDCs, whereas canine MoDCs induced Th1/Th17 responses, with increased CD4 T cells producing IFN-γ and IL-17A simultaneously. Each pattern of cellular response may contribute to host susceptibility, helping to understand the differences in B. canis virulence between these two hosts. In addition, other aspects of canine immunology are unveiled by highlighting the participation of IL-17A-producing canine MoDCs and CD4 T cells producing IFN-γ and IL-17A.
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http://dx.doi.org/10.1016/j.cimid.2018.11.017 | DOI Listing |
J Immunother Cancer
March 2025
St. John's Institute of Dermatology, School of Basic & Medical Biosciences & KHP Centre for Translational Medicine, King's College London, London, UK
Background: Anti-human epidermal growth factor receptor 2 (HER2) IgG1-based antibody therapies significantly improve cancer prognosis, yet intrinsic or acquired resistance to fragment antigen-binding (Fab)-mediated direct effects commonly occurs. Most resistant tumors retain antigen expression and therefore remain potentially targetable with anti-HER2 therapies that promote immune-mediated responses. Tumor-antigen-specific IgE class antibodies can mediate powerful immune cell-mediated effects against different cancers and have been shown to activate IgE Fc receptor-expressing monocytes.
View Article and Find Full Text PDFGut
March 2025
Department of Gastroenterology, Shanghai Tenth People's Hospital, Shanghai, China
Background: GPR171 suppresses T cell immune responses involved in antitumour immunity, while its role in inflammatory bowel disease (IBD) pathogenesis remains unclear.
Objective: We aimed to investigate the role of GPR171 in modulating CD4 T cell effector functions in IBD and evaluate its therapeutic potential.
Design: We analysed GPR171 expression in colon biopsies and peripheral blood samples from patients with IBD and assessed the impact of GPR171 on CD4 T cell differentiation through administration of its endogenous ligand (BigLEN).
Background: The pathogenesis of female pelvic floor polypropylene mesh complications is unclear as trials evaluating explanted mesh have not included asymptomatic controls.
Objectives: To compare explanted polypropylene mesh from those with and without mesh complications to determine the pathogenesis of the complications.
Methods: Between August 2019 and July 2020 66 participants attending Wesley and Royal Brisbane and Women's Hospital Urogynecology department with mesh complications and 15 undergoing repeat prolapse and/or continence surgery after prior polypropylene mesh implantation were included.
Cell Rep
March 2025
Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montréal, QC, Canada; Département de médicine, Université de Montréal, Montréal, QC, Canada. Electronic address:
Ansari et al. identified a subset of CD4 T cells (CXCR5PD-1) resembling T follicular helper (Tfh) cells in patients with severe dengue. This subset helps B cell responses via IL-21 and can also differentiate into cytotoxic CD4 T cells.
View Article and Find Full Text PDFCell Rep
March 2025
Vaccine Immunology Laboratory, National Institute of Immunology, New Delhi 110067, India. Electronic address:
Dengue-virus-induced humoral immunity can increase the risk of severe disease, but the factors influencing this response are poorly understood. Here, we investigate the contribution of CD4 T cells to B cell responses in human dengue infection. We identify a dominant peripheral PD-1 T cell subset that accumulates in severe patients and could induce B cell differentiation via interleukin-21 (IL-21)-related pathway.
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