European Journal of Immunology

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

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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”}]]

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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”}]]

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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”}]]

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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

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”}]]

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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

Epigenetic Regulation of CD8+ Effector T Cell Differentiation by PDCD5. [[{“value”:”Lixue Jin, Xin Zhang, Jingyi Wang, Yujia Wang, Ke Wang, Zhuolin Wang, Pingzhang Wang, Xiuyuan Sun, Jie Hao, Rong Jin, Dan Lu, Qing Ge”}]]

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In CD8+ T cells, PDCD5 is an activation-induced molecule that interacts with PRDM9, thereby promoting its nuclear translocation and facilitating the H3K4me3 modification of genes associated with effector differentiation. ABSTRACT Epigenetic modification plays a crucial role in establishing the transcriptional program that governs the differentiation of CD8+ effector T cells. However, the mechanisms by which … Read more

ICAM‐1 Is Overexpressed by Cancers and Negatively Impacts Antibody‐Based Therapies Including Antibody–Drug Conjugates. [[{“value”:”J. Bradford Kline, Luigi Grasso, Nicholas C. Nicolaides”}]]

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Tumor-produced ICAM-1 protein binds to IgG1 antibodies and suppresses their antibody-dependent cellular (ADCC) and complement-dependent (CDC) cytotoxicity against antigen-positive cells via reduced engagement with CD16a receptors on immune effector cells and C1q complement protein. This interaction also reduces antibody internalization that negatively affects antibody–drug conjugate cytotoxicity. ABSTRACT Humoral immunity utilizes antibodies and immune effector cells to … Read more

JAK Inhibitors and B Cell Function: A Comparative Study of Their Impact on Plasma Cell Differentiation, Cytokine Production, and Naïve B Cell Activation. [[{“value”:”Wenqi Huang, Charlotte de Vries, Ravi Kumar Sharma, Kittikorn Wangriatisak, Katerina Chatzidionysiou, Vivianne Malmström, Caroline Grönwall”}]]

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JAK inhibitors (baricitinib, tofacitinib, upadacitinib), except for filgotinib, significantly reduce plasmablast differentiation but only partly inhibit activation of naïve B cells and exert a more modest effect on TNF and IL-8 production. Unlike other JAK inhibitors, filgotinib selectively inhibits STAT5 phosphorylation without affecting STAT3 phosphorylation in response to IL-21. ABSTRACT B cells play a crucial … Read more

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