Immunity

Mitochondria reactive oxygen species signaling-dependent immune responses in macrophages and T cells Mitochondrial reactive oxygen species (mtROS) serve as critical signaling molecules that regulate immunity. Chandel et al. review the spectrum of mtROS effects, ranging from essential roles in innate immune activation and T cell differentiation to pathological inflammation and T cell dysfunction.

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From complexity to consensus: A roadmap for neutrophil classification Neutrophils are highly dynamic immune cells with diverse phenotypes shaped by development, tissue-specific signals, and disease contexts. This perspective proposes a four-tiered framework integrating maturation, tissue localization, and function to standardize neutrophil research, improve cross-study comparisons, and support the discovery of targeted therapies in inflammation and immune-related diseases.

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Polyamines regulate adaptive antitumor immunity by functional specialization of regulatory T cells @cp-immunity.bsky.social
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Mutations in MLL3 promote breast cancer progression via HIF1α-dependent intratumoral recruitment and differentiation of regulatory T cells Mutations in MLL3, encoding the histone methyltransferase MLL3/KMT2C, are frequent in various cancer types. Boutet, Nishitani, et al. show that the loss of MLL3 stabilizes HIF1α, which induces expression of the chemokine CCL2 and promotes infiltration of CCR2+ Treg cells into breast tumors, wherein HIF1α promotes differentiation into ICOS+GITR+ highly suppressive Treg cells.

Online now: Mutations in MLL3 promote breast cancer progression via HIF1α-dependent intratumoral recruitment and differentiation of regulatory T cells

Polyamines regulate adaptive antitumor immunity by functional specialization of regulatory T cells Bündgen et al. reveal that polyamines in the tumor environment shift Treg cells toward suppression via CK2 signaling. Blocking this pathway reprograms Treg cells to support tissue repair and antitumor immunity. These findings highlight a potential strategy to rewire immune responses and improve cancer therapies.

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Innate-like memory T cells rapidly emerge in humans after gene therapy for SCID-X1 test Vasandan et al. leverage a gene therapy study of X-linked severe combined immunodeficient individuals to longitudinally examine human immune development. They find early emergence of antigen-independent, innate-like memory T cells that are epigenetically poised for effector responses. These cells likely represent an innate-like mechanism of host protection in humans that arises before adequate development of adaptive immunity.

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Re-wilding the microbiota of lab mice enhances preclinical modeling of human immune responses. #RehermanLab shows long-term stability of these models over years with ⬆️myeloid, NK, T, B @cp-immunity.bsky.social
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Balancing nutrient uptake and host defense in the intestine facilitated by a Gasdermin-D-mediated epithelial-immune circuit @cp-immunity.bsky.social
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Asynchronous aging and turnover of human circulating and tissue-resident memory T cells across sites Human memory T cells persist in tissues as circulating and tissue-resident populations. Lam et al. reveal asynchronous aging of T cells across sites and subsets. Splenic memory T cells are longer-lived compared with mucosal sites and blood. Tissue-resident T cells demonstrate stable persistence, avoiding the acquisition of immunosenescent features seen in circulating subsets.

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Naturalized immune responses are stable over years in a colony of laboratory mice with wild-derived microbiota The transfer of microbiota and pathogens from wild mice to genetically tractable laboratory mice has been shown to enhance modeling of human immune responses in preclinical studies. However, the long-term stability of the transferred complex microbiota and the induced immune phenotype in a standard laboratory mouse colony are not known. Oh et al. demonstrate that microbiota from wild mice maintain their composition and biodiversity over multiple years in a laboratory mouse colony, with increased myeloid cell numbers and immune cell function across organs. This phenotype can be transferred to adult lab mice, creating a sharable resource for preclinical research.

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Mitochondrial complex IV remodeling plays a key role in how macrophages adapt to their surroundings—findings with major implications for #immunotherapy. Check out the newest study from Penn Medicine (@pennmedicine.bsky.social) researchers published in Immunity (@cp-immunity.bsky.social).

Gasdermin-D-mediated epithelial-immune circuit synchronizes nutrient absorption and host defense in the small intestine Precisely how diet regulates intestinal immunity and barrier function remains underexplored. Yu et al. identify a link between nutrient signals and host defense directed by diet-induced, GSDMD-mediated epithelial-immune co-adaptation. This study contributes to further understanding of the deleterious effects of nutritional imbalances and disturbed eating patterns on intestinal homeostasis.

Online now: Gasdermin-D-mediated epithelial-immune circuit synchronizes nutrient absorption and host defense in the small intestine

Cell Symposia

Check out the program for #cellpressevents.bsky.social, Neuro-immune axis: Charting the periphery, in partnership with the Allen Discovery Center for Neuroimmune Interactions. Join us NYC for cutting-edge neuroimmune science. http://dlvr.it/TM586n

Gasdermin C cleavage by Cathepsin S modulates Rab7 vesicles in intestinal epithelial cells to amplify anti-helminth immunity Pandey et al. identify Cathepsin S (CTSS) as the direct protease that cleaves Gasdermin C (GsdmC) in the intestine. Type 2 immune-promoting microbes trigger CTSS-dependent GsdmC activation in intestinal epithelial cells, targeting Rab7+ vesicles, altering lipid metabolism, and modulating anti-helminth immunity, revealing a non-pyroptotic function of GsdmC in mucosal immune regulation.

Online now: Gasdermin C cleavage by Cathepsin S modulates Rab7 vesicles in intestinal epithelial cells to amplify anti-helminth immunity

Induction of IL-10-producing type 2 innate lymphoid cells by allergen immunotherapy is associated with clinical response (Immunity 54, 291–307.e1–e7; February 9, 2021)

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Register early and save

Don’t miss @uofcalifornia.bsky.social Päivi Pajukanta’s talk on cell-type level mechanisms for cardiometabolic disease in Mexicans @CellSymposia #CSPrecisionGen25. Early registration ends: July 25, 2025! http://dlvr.it/TM36Dg

Epigenetic silencing of interleukin-10 by host-derived oxidized phospholipids supports a lethal inflammatory response to infections Phagocytes initiate immunity to invading microorganisms by detecting pathogen-associated molecular patterns via pattern recognition receptors. Pathoge…

Host-derived oxidized phospholipids (oxPLs) shut down IL-10 via AKT-EZH2 signaling, leading to lethal inflammation. Blocking oxPLs revives IL-10 and boosts survival. Great mechanistic insight from ‪the awesome @lozanzi.bsky.social‬ lab in ‪@cp-immunity.bsky.social‬: doi.org/10.1016/j.im... 🧪

ft. @megclarks, W. Mowel, @MFMich1, L. Joannas, J. Wright, I. Erickson, J. Henao-Mejia (@pennpathlabmed.bsky.social), L. Johnson, @andyjminn (@i3h-upenn.bsky.social), @rakez_krish, @delafuentelab.bsky.social (@PennPsych) & @ksimeono (@PennVet) @cp-immunity.bsky.social www.cell.com/immunity/abs...

Host-derived oxidized phospholipids accumulate upon microbial encounter, epigenetically suppress IL-10, and exacerbate harmful inflammation @cp-immunity.bsky.social
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Congratulations to @lozanzi.bsky.social and team on this cool story @cp-immunity.bsky.social: "Epigenetic silencing of interleukin-10 by host-derived oxidized phospholipids supports a lethal inflammatory response to infections." Honored to have made a small contribution to such important work.

CINTER-seq enables in situ capture and multimodal profiling of interacting cells in living mice, uncovering specific LAG3-MHC II-mediated CD4+ T cell-cancer cell interactions & tumor-reprogrammed neutrophils
www.cell.com/immunity/ful... @cp-immunity.bsky.social

Fungal cues, fibrotic consequences: Commensal sensing by alveolar macrophages promotes pulmonary fibrosis In a recent issue of Immunity, Qiu et al. uncover a pivotal role for commensal fungi in promoting lung fibrosis, showing that their interaction with alveolar macrophages triggers a profibrotic transcr...

Fungal cues, fibrotic consequences:

Highlight of @cp-immunity.bsky.social work uncovering role for commensal fungi in lung fibrosis, showing that their interaction w/alveolar macrophages triggers profibrotic transcriptional program through Dectin-1-Raf1 signaling axis
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This is so cool, congrats @lozanzi.bsky.social and team! Important implications for infection and IBD

Epigenetic silencing of interleukin-10 by host-derived oxidized phospholipids supports a lethal inflammatory response to infections Upon pathogen detection, phagocytes trigger immunity. This process induces tissue stress and the formation of host-derived molecules that further tune immune responses. We show that host-derived oxidi...

#EpigeneticPower! 💥 #NewPaperAlert! We show @cp-immunity.bsky.social that endogenous oxidized lipids decide whether host survives or dies during #sepsis, #ARDS, or Staph infection! Ox lipids bind & inhibit #AKT, boosting inhibitory H3K27 methylation via EZH2 & blocking #IL10!

Epigenetic silencing of interleukin-10 by host-derived oxidized phospholipids supports a lethal inflammatory response to infections Upon pathogen detection, phagocytes trigger immunity. This process induces tissue stress and the formation of host-derived molecules that further tune immune responses. We show that host-derived oxidized phospholipids accumulate upon microbial encounter, epigenetically suppress IL-10, and exacerbate harmful inflammation. Thus, targeting oxPLs represents a therapeutic strategy to treat deranged inflammation after infection.

Online now: Epigenetic silencing of interleukin-10 by host-derived oxidized phospholipids supports a lethal inflammatory response to infections

CINTER-seq: Chemical profiling reveals interaction-dependent cell landscapes and gene signatures in vivo Physical cellular interactions are crucial yet remain challenging to investigate in vivo. Deng et al. develop CINTER-seq, a chemical tool enabling in situ capture and multimodal profiling of interacting cells in living mice, uncovering specific LAG3-MHC class II-mediated CD4+ T cell-cancer cell interactions and tumor-reprogrammed neutrophils with pro-tumor functions.

Online now: CINTER-seq: Chemical profiling reveals interaction-dependent cell landscapes and gene signatures in vivo

Systems analysis of clinical malaria reveals proteomic perturbation and innate-adaptive crosstalk linked to disease severity While the immune response to Plasmodium falciparum malaria has been studied extensively, the circulating proteome and its cellular origins remain poorly characterized. Lautenbach et al. address this b...

Proud co‑author on @cp-immunity.bsky.social study by Julius Lautenbach, @chrissundling.bsky.social & Team Färnert w/ HPA & @scilifelab.se. We integrate plasma proteome dynamics (1500 proteins) + scRNA-seq in acute malaria, identifying severity markers & exploring immune-cell communication.

RORγt+ dendritic cells and regulatory T cells: A couple hiding in the shadows The induction of CD4+Foxp3+ regulatory T cells (pTreg cells) in the intestine is important for preventing allergic and inflammatory disease, but which…

A short spotlight in @cp-immunity.bsky.social by Brian Kelsall.
on the recently described RORγt+ DCs and their function in inducing intestinal tolerance.
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Integration of plasma proteomics and scRNA-seq in 72 patients reveal molecular patterns linked to disease severity, immune regulation, and tissue origin in clinical malaria @cp-immunity.bsky.social
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Autoreactive leptomeningeal B cells drive neuroinflammation by engaging pathogenic T cells and amplifying a local pro-inflammatory cascade
www.cell.com/immunity/ful... @cp-immunity.bsky.social