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.

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.

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.

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.

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.

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.

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.

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.

Spatiotemporal aspects of bystander killing triggered by bispecific antibodies: (1) Resting T-cells recognize HER2+ tumors via CD3xHER2 bsAbs. (2) Local T-cell activation induces direct HER2⁺ tumor killing and IFNγ/TNFα release. (3) IFNγ/TNFα mediate paracrine killing of HER2⁻ cells. (4) HER2⁻ cells are eliminated in mixed (A) and distant (B) areas.

Here we show that CST and SHLD are required for CSR, while SHLD1-CTC1 interaction via the SHLD1 LDLP motif is dispensable. Mechanistically, we show that CTC1 and SHLD1 are epistatic during CSR, preventing genetic instability, exacerbated DSB end-resection, and microhomology-mediated end-joining at Igh switching sites. Created in Biorender.com.

Metabolic antagonism in the TME suppresses CD8⁺ T cell function by depleting essential nutrients and generating toxic byproducts. Metabolic symbiosis between tumor cells and TAMs fosters an immunosuppressive microenvironment. Disrupting metabolic interactions can overcome immune suppression, boost antitumor immunity, and enhance immunotherapy efficacy.

T-cell recognition of microbiota-derived epitopes is key to immune homeostasis. Here, we used an unbiased screening platform to identify novel immunogenic epitopes from Akkermansia muciniphila and Bacteroides thetaiotaomicron. We demonstrated that these epitopes are conserved across multiple other bacterial strains, suggesting their potential relevance in broader immune interactions.

The evolution of the concept of the immune system from a set of composed cells and tissue that defend the host from exogenous agents into a system that has regulatory and homeostatic functions determined by the interaction with microorganisms as a functional part of an extended immune system, that we call symmunobiome.

Dimethyl fumarate (DMF) inhibits T-cell proliferation and induces apoptosis by depleting glutathione (GSH) and accumulating reactive oxygen species (ROS). Here, we show that DMF-induced oxidative stress disrupts multiple cell-signaling pathways, including MYC, leading to cell cycle arrest and impaired proliferative responses in activated T-cells.

The supernatant of M. tuberculosis-stimulated B cells promotes monocyte polarization toward an anti-inflammatory CD16⁺CD163⁺CD206⁺PD-L1⁺ phenotype via an IL-6/STAT3 pathway. Confirmed with B cells from TB patients, this pathway impairs monocyte proinflammatory functions and may contribute to immune suppression in tuberculosis. Created in BioRender. Neyrolles, O. (2025) https://BioRender.com/930ras3

Analysis of the T-cell epitope landscape of SARS-CoV-2 suggests T-cell intrinsic factors as likely modulators of disease severity and that the capacity of MHC-peptide presentation remains stable among circulating SARS-CoV-2 viral strains.

Probiotics administered to pregnant mice led to increased frequencies of IL17-committed Vγ6⁺ γδ T cells in the neonatal lung. This highlights a microbiota-sensitive pathway where maternal probiotics enhance γδ17 commitment in the perinatal lung.

Multiple immunizations of mice with Plasmodium berghei radiation-attenuated sporozoites (Pb RAS) induce durable protective immunity, provided that 1° sporozoite (spz) challenge occurs early or within 10 months following the most recent RAS boost immunization. Delaying 1° challenge results in parasitemia. Pb RAS develops partially into early liver stages, is unable to progress to blood-stage parasites, and is taken up and presented by APCs to naïve CD8⁺T cells, which differentiate into CD8⁺T_E/EM cells to eliminate infectious parasites. An early 1° challenge enhances CD8⁺T_E/EM survival and functional properties necessary for durable protective immunity. By contrast, in the absence of an early infectious spz challenge, activated CD8⁺T cells exhibit decreased survival and functional attributes, resulting in a gradual loss of protection.