Minor Splicing Factor RNPC3 Is Essential for the Germinal Center B Cell Response. [[{“value”:”Jing Wang, Gui‐Xin Ruan, Yuxing Li, Xiong Xiao, Zhijian Zhu, Wenjing Chen, Hengjun Huang, Rui Zhang, Ruisi Wang, Meiyuan Chen, Ling Guo, Yan Li, Shengli Xu, Xijun Ou”}]]

RNPC3, as a unique minor spliceosome component, plays a critical role in T cell-dependent immune response. By facilitating minor intron splicing, RNPC3 promotes the proliferation of activated B cells and prevents their apoptosis, thereby supporting the formation of early germinal center B cells. ABSTRACT Germinal center (GC) response ensures the generation of diverse and high-affinity … Read more

Modulation of Host Immunity by Microbiome‐Derived Indole‐3‐Propionic Acid and Other Bacterial Metabolites. [[{“value”:”Burkhard Schütz, Felix F. Krause, R. Verena Taudte, Mario M. Zaiss, Maik Luu, Alexander Visekruna”}]]

The gut commensal Clostridium sporogenes metabolizes dietary tryptophan into indole-3-propionic acid (IPA). In this review, we highlight recent findings suggesting that IPA acts as an effective signaling molecule, modulating the function of Th17 lymphocytes and resulting in protection against intestinal inflammation. ABSTRACT In recent years, we have witnessed a rapidly growing interest in the intricate … Read more

Interleukin‐8/Matrix Metalloproteinase‐9 Axis Impairs Wound Healing in Type 2 Diabetes through Neutrophil Extracellular Traps‐Fibroblast Crosstalk. [[{“value”:”Dimitrios Tsilingiris, Anastasia‐Maria Natsi, Efstratios Gavriilidis, Christina Antoniadou, Ioanna Eleftheriadou, Ioanna A. Anastasiou, Anastasios Tentolouris, Evangelos Papadimitriou, Evgenios Eftalitsidis, Panagiotis Kolovos, Victoria Tsironidou, Alexandra Giatromanolaki, Maria Koffa, Nikolaos Tentolouris, Panagiotis Skendros, Konstantinos Ritis”}]]

Neutrophil extracellular traps (NETs) in type 2 diabetes induce a pro-fibrotic but functionally impaired phenotype in cutaneous fibroblasts, associated with collagen breakdown by NET-bound MMP-9. IL-8 released in NETs promotes its own expression in both neutrophils/fibroblasts and neutrophil MMP-9 production, creating positive feedback loops that hinder wound healing. ABSTRACT Neutrophils interact with and activate fibroblasts … Read more

PLC and PAD2 Regulate Extracellular Calcium‐Triggered Release of Macrophage Extracellular DNA Traps. [[{“value”:”Neha Mishra, Magdalena Mohs, Nico Wittmann, Stefan Gross, Paul R. Thompson, Lukas Bossaller”}]]

Extracellular calcium induces MET release from human macrophages. Concurrently, extracellular calcium activates the NLRP3 inflammasome. Citrullinated histones, MMP12, MPO and ASC specks are bound to METs and are released by rupture of the plasma membrane, where they exhibit bactericidal properties. ABSTRACT Macrophages can respond to infection or cellular stress by forming inflammasomes or by releasing … Read more

Metabolic Reprogramming in Stromal and Immune Cells in Rheumatoid Arthritis and Osteoarthritis: Therapeutic Possibilities. [[{“value”:”Órlaith C. Henry, Luke A. J. O’Neill”}]]

Immune cells and stromal cells undergo metabolic reprogramming in both rheumatoid and osteoarthritis. This review summarises current evidence on the metabolic changes within and the crosstalk between immune and stromal cells in these diseases. In addition, we explore the therapeutic potential of targeting metabolic processes for the treatment of arthritis. ABSTRACT Metabolic reprogramming of stromal … Read more

IgA2 ACPA Drives a Hyper‐Inflammatory Phenotype in Macrophages via ATP Synthase and COX2. [[{“value”:”Luís Almeida, Alice Bacon, Mohan Ghorasaini, Alwin J. van der Ham, René E. M. Toes, Martin Giera, Bart Everts”}]]

IgA autoantibodies have been implicated in promoting inflammation associated with rheumatoid arthritis by engaging Fc receptors on myeloid cells. However, underlying mechanisms are still poorly defined. Here, we identified immune complexed IgA2, but not IgA1, to induce hyper-inflammatory macrophages, and that it is dependent on ATP synthase and COX2 activity. ABSTRACT IgA can form immune … Read more

Expansion of Interleukin‐22‐Producing Type 3 Innate Lymphoid Cells in the Gut of Tristetraprolin‐Deficient Mice. [[{“value”:”Bérengère de de Toeuf, Maxime Melchior, Caroline La, Aresio Villanueva Alcantara, Abdulkader Azouz, Vincent Martens, Céline La, Ingrid Dubois, Sylvie Vande Velde, Lara Meyer, Muriel Nguyen, Séverine Thomas, Frédérick Libert, Laure Dumoutier, Perry J. Blackshear, Stanislas Goriely”}]]

TTP controls the mRNA stability of multiple inflammatory cytokines. Despite a multiorgan inflammatory phenotype, TTP-deficient mice are protected from experimental colitis, in part, through the expansion of IL-22-producing ILC3 in the gut. ABSTRACT Tristetraprolin (TTP, encoded by Zfp36) is an RNA-binding protein that plays a major role in the control of inflammation. Zfp36−/− mice spontaneously … Read more

Monocyte‐Platelet Aggregates Are Major Source of BDNF after Bacterial Stimulation of Human Peripheral Blood Immune Cells. [[{“value”:”Fabien Sarcletti, Marco Dijmarescu, Michael Eigenschink, Nadja Wukowits, Barbara Oehler, Tanja Mayer, Sarah Pell, Anastasia Tandecki, David Seki, Andreas Spittler, David Berry, Angelika Berger, Lukas Wisgrill”}]]

Bacterial antigens primarily induce BDNF release from platelets interacting with monocytes in PBMCs. This interplay underscores how immune-blood cell complexes shape BDNF levels which may impact early human development. ABSTRACT The gut microbiota and the immune system are closely connected, influencing early-life brain development. Brain-derived neurotrophic factor (BDNF), crucial for neuronal development, has been demonstrated … Read more

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