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Lifelong partners: Gut microbiota-immune cell interactions from infancy to old age

Mucosal immunology 2025年第3期18卷 509-523页

作者： Brown, Julia A. Bashir, Hilal Zeng, Melody Y. Gale and Ira Drukier Institute for Children's Health Weill Cornell Medicine New York 10065 NY United States Department of Pediatrics Weill Cornell Medicine New York 10065 NY United States Immunology and Microbial Pathogenesis Program Weill Cornell Graduate School New York 10065 NY United States

Our immune system and gut microbiota are intricately coupled from birth, both going through maturation during early life and senescence during aging almost in a synchronized fashion. The symbiotic relationship between the human host and microbiota is critically dependent on a healthy immune system to keep our microbiota in check, while the microbiota provides essential functions to promote the development and fitness of our immune system. The partnership between our immune system and microbiota is particularly important during early life, when microbial ligands and metabolites shape the development of the immune cells and immune tolerance;during aging, having sufficient beneficial gut bacteria is critical for the maintenance of intact mucosal barriers, immune metabolic fitness, and strong immunity against pathogens. The immune system during childhood is programmed, with the support of the microbiota, to develop robust immune tolerance, and limit autoimmunity and metabolic dysregulation, which are prevalent during aging. This review comprehensively explores the mechanistic underpinnings of gut microbiota-immune cell interactions during infancy and old age, with the goal to gain a better understanding of potential strategies to leverage the gut microbiota to combat age-related immune decline. © 2025

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Cytotoxic innate lymphoid cells sense cancer cell-expressed interleukin-15 to suppress human and murine malignancies (vol 23, pg 904, 2022)

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NATURE immunology 2022年第8期23卷 1285-1285页

作者： Kansler, Emily R. Dadi, Saida Krishna, Chirag Nixon, Briana G. Stamatiades, Efstathios G. Liu, Ming Kuo, Fengshen Zhang, Jing Zhang, Xian Capistrano, Kristelle Blum, Kyle A. Weiss, Kate Kedl, Ross M. Cui, Guangwei Ikuta, Koichi Chan, Timothy A. Leslie, Christina S. Hakimi, A. Ari Li, Ming O. Immunology Program Memorial Sloan Kettering Cancer Center New York NY USA Louis V. Gerstner Jr. Graduate School of Biomedical Sciences Memorial Sloan Kettering Cancer Center New York NY USA Immunology and Microbial Pathogenesis Graduate Program Weill Cornell Graduate School of Medical Sciences Cornell University New York NY USA Computational and Systems Biology Program Memorial Sloan Kettering Cancer Center New York NY USA Human Oncology and Pathogenesis Program Memorial Sloan Kettering Cancer Center New York NY USA Department of Immunology and Microbiology University of Colorado Anschutz Medical Campus Aurora CO USA Laboratory of Immune Regulation Department of Virus Research Institute for Frontier Life and Medical Sciences Kyoto University Kyoto Japan Department of Urology Memorial Sloan Kettering Cancer Center New York NY USA

Malignancy can be suppressed by the immune system. However, the classes of immunosurveillance responses and their mode of tumor sensing remain incompletely understood. Here, we show that although clear cell renal cell carcinoma (ccRCC) was infiltrated by exhaustion-phenotype CD8+T cells that negatively correlated with patient prognosis, chromophobe RCC (chRCC) had abundant infiltration of granzyme A-expressing intraepithelial type 1 innate lymphoid cells (ILC1s) that positively associated with patient survival. Interleukin-15 (IL-15) promoted ILC1 granzyme A expression and cytotoxicity, and IL-15 expression in chRCC tumor tissue positively tracked with the ILC1 response. An ILC1 gene signature also predicted survival of a subset of breast cancer patients in association with IL-15 expression. Notably, ILC1s directly interacted with cancer cells, and IL-15 produced by cancer cells supported the expansion and anti-tumor function of ILC1s in a murine breast cancer model. Thus, ILC1 sensing of cancer cell IL-15 defines an immunosurveillance mechanism of epithelial malignancies.

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Metabolism along the life journey of T cells

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Life Metabolism 2023年第1期2卷 24-32页

作者： Min Peng Ming O.Li Department of Basic Medical Sciences School of MedicineTsinghua UniversityBeijing 100084China Institute for Immunology Tsinghua UniversityBeijing 100084China Tsinghua-Peking Center for Life Sciences Beijing 100084China Beijing Key Laboratory for Immunological Research on Chronic Diseases Tsinghua UniversityBeijing 100084China Immunology Program Sloan Kettering InstituteMemorial Sloan Kettering Cancer CenterNew YorkNY 10065USA Immunology and Microbial Pathogenesis Program Weill Cornell Graduate School of Medical SciencesCornell UniversityNew YorkNY 10065USA

T cells are one of few cell types in adult mammals that can proliferate extensively and differentiate diversely upon stimulation,which serves as an excellent example to dissect the metabolic basis of cell fate *** the last decade,there has been an explosion of research into the metabolic control of T-cell *** roles of common metabolic pathways,including glycolysis,lipid metabolism,and mitochondrial oxidative phosphorylation,in T-cell responses have been well characterized,and their mechanisms of action are starting to *** this review,we present several considerations for T-cell metabolism-focused research,while providing an overview of the metabolic control of T-cell fate decisions during their life *** try to synthesize principles that explain the causal relationship between cellular metabolism and T-cell fate *** also discuss key unresolved questions and challenges in targeting T-cell metabolism to treat disease.

关键词： T cells immunometabolism glycolysis OXPHOS FAO acetyl-CoA

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MEF2C regulates osteoclastogenesis and pathologic bone resorption via c-FOS

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Bone Research 2021年第1期9卷 50-62页

作者： Takayuki Fujii Koichi Murata Se-Hwan Mun Seyeon Bae Ye Ji Lee Tannia Pannellini Kyuho Kang David Oliver Kyung-Hyun Park-Min Lionel B.Ivashkiv Arthritis and Tissue Degeneration Program and David Z.Rosensweig Genomics Research Center Hospital for Special SurgeryNew YorkNY 10021USA Department of Orthopaedic Surgery Kyoto University Graduate School of MedicineSakyoKyoto 606-8507Japan Department of Advanced Medicine for Rheumatic Diseases Kyoto University Graduate School of MedicineSakyoKyoto 606-8507Japan Department of Biology Chungbuk National UniversityCheongju 28644Republic of Korea BCMB Allied Program Weill Cornell Graduate School of Medical ScienceNew YorkNY 10021USA Immunology and Microbial Pathogenesis Program Weill Cornell Graduate School of Medical ScienceNew YorkNY 10021USA

Osteoporosis is a metabolic bone disease with dysregulated coupling between bone resorption and bone formation,which results in decreased bone mineral *** MEF2C locus,which encodes the transcription factor MADS box transcription enhancer factor 2,polypeptide C(MEF2C),is strongly associated with adult osteoporosis and osteoporotic *** the role of MEF2C in bone and cartilage formation by osteoblasts,osteocytes,and chondrocytes has been studied,the role of MEF2C in osteoclasts,which mediate bone resorption,remains *** this study,we identified MEF2C as a positive regulator of human and mouse osteoclast *** decreased MEF2C expression resulted in diminished osteoclastogenesis,ectopic expression of MEF2C enhanced osteoclast *** transcriptomic and bioinformatic approaches,we found that MEF2C promotes the RANKL-mediated induction of the transcription factors c-FOS and NFATc1,which play a key role in ***,MEF2C binds to FOS regulatory regions to induce c-FOS expression,leading to the activation of NFATC1 and downstream *** deletion of Mef2c in mice resulted in increased bone mass under physiological conditions and protected mice from bone erosion by diminishing osteoclast formation in K/BxN serum induced arthritis,a murine model of inflammatory *** findings reveal direct regulation of osteoclasts by MEF2C,thus adding osteoclasts as a cell type in which altered MEF2C expression or function can contribute to pathological bone remodeling.

关键词： osteoclast MEF2C pathologic

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Paneth Cells Provide a Unique Source of EGF for Intestinal Epithelium in Radiation Injury That Is Dispensable in Gvhd.

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Transplantation and Cellular Therapy 2025年第2期31卷 S55-S56页

作者： Winston Yun-Han Chang Viktor Arnhold Ya-Yuan Fu Marco Calafiore Shuichiro Takashima Riley Outen Anastasiya Egorova Jason Kuttiyara Chen Liu Alan M. Hanash Department of Medicine Memorial Sloan Kettering Cancer Center New York NY Immunology and Microbial Pathogenesis Graduate Program Weill Cornell Medical College New York NY Immunology and Microbial Pathogenesis Graduate Program Weill Cornell Medicine New York NY Department of Pathology Yale School of Medicine New Haven CT Department of Medicine Adult Bone Marrow Transplant Service Memorial Sloan Kettering Cancer Center New York NY Department of Medicine Weill Cornell Medical College New York NY

Paneth cells (PCs) are a secretory epithelial population located in small intestine (SI) crypts. PCs produce growth factors within the intestinal stem cell (ISC) niche, including WNT3, DLL1 and EGF, that maintain the intestinal epithelium. In murine models of acute GVHD, reductions in both ISCs and PCs has been reported. In patients with GVHD, PC loss has also been observed and its severity is correlated with poor clinical prognosis. We therefore asked if the loss of PCs and their niche function led to ISC loss, intestinal pathology, and overall GVHD outcomes. To investigate, we treated Lyz1 DTR B6 mice with diphtheria toxin to ablate PCs prior to a MHC-mismatch BMT from *** mice. The elimination of PCs in the SI (Fig 1A) had no impact on survival, clinical scores, and weight loss versus WT mice (Fig 1B). PC ablation also did not affect ISC and crypt loss (not shown). To determine if MHC-mismatched GVHD severity overwhelmed PC support of the SI and overall outcomes, we performed a minor-antigen-mismatched 129-into-B6 BMT. Again, PC ablation had no effect on survival, scoring and weight loss (Fig 1C), indicating experimental GVHD was not driven by PC maintenance of intestinal crypts. Given the lack of impact from PC ablation on crypt injury in GVHD, we examined the expression of niche factors in crypts from WT and Lyz1 DTR BMT recipients. While GVHD reduced the expression of Dll1 and WNT3, PC ablation had no further effect (Fig 2A) . However, PC ablation reduced crypt EGF expression (Fig 2A). The persistence of niche factors despite PC ablation suggested other potential sources. Indeed, scRNA-sequencing analysis of crypts (Fig. 2CB) identified other epithelial populations expressing these factors. Expression of Wnt3 by non-PC cells was validated by smFISH staining (Fig 2C), and their contribution appeared to increase during GVHD (Fig 2D). These finding indicated that other cells besides PCs may support the ISC niche. While PCs were a non-redundant source of EGF, t

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Keynote Lecture 1 A non-canonical pathway of cross-presentation disables self/non-self discrimination

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Molecular immunology 2022年 150卷 14-15页

作者： J. Magarian Blander The Jill Roberts Institute for Research in Inflammatory Bowel Disease Weill Cornell Graduate School of Medical Science Weill Cornell Medicine Cornell University New York NY 10021 USA Joan and Sanford I. Weill Department of Medicine Weill Cornell Graduate School of Medical Science Weill Cornell Medicine Cornell University New York NY 10021 USA Department of Microbiology and Immunology Weill Cornell Graduate School of Medical Science Weill Cornell Medicine Cornell University New York NY 10021 USA Sandra and Edward Meyer Cancer Center Weill Cornell Graduate School of Medical Science Weill Cornell Medicine Cornell University New York NY 10021 USA Immunology and Microbial Pathogenesis Program Weill Cornell Graduate School of Medical Science Weill Cornell Medicine Cornell University New York NY 10021 USA

The classic pathway of MHC class I (MHC-I) presentation by dendritic cells (DC) is critical to initiate immunity against microbial pathogens. For viruses that do not infect DC or when the antigen presentation functions of infected DC have been compromised, cross-presentation ensures the mobilization of an antiviral CD8 T cell response. Cross-presentation is an adaptation of the classical pathway of MHC-I presentation that DC specialize in to present peptides derived from extracellular antigens by MHC-I molecules. Understanding the mechanisms and regulation of cross-presentation has direct implications to the urgent need for developing T cell vaccines against intracellular pathogens such as HIV, Mycobacterium tuberculosis and malaria. We have shown that the cross-presentation of particulate antigens is highly dependent on Toll-like receptor (TLR) signaling in phagosomes. We reported that MHC-I molecules accumulate in endosomal recycling compartments (ERC) in DC and serve to supply phagosomes with MHC-I molecules for loading with peptides during cross-presentation. Mechanistically, MyD88-dependent TLR signals drive IκB-kinase (IKK)2-mediated phosphorylation of phagosome-associated synaptosome associated protein 23 (SNAP23). Phospho-SNAP23 stabilizes SNARE complexes between the ERC and phagosomes and orchestrates their fusion. As a result, ERC-resident MHC-I molecules are delivered specifically to phagosomes containing TLR ligands favoring the cross-presentation of microbial over self peptides. I will review this pathway and present unpublished data showing how subcellular mislocalization of MHC-I molecules under specific circumstances disrupts the TLR-mediated control of cross-presentation and disables the ability to discriminate self from non-self peptides.

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PP 4.16 – 00188 Investigating the Role of Naïve CD4+ T-cells as a CTL Resistant Sanctuary for Intact HIV Proviruses

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Journal of Virus Eradication 2022年 8卷

作者： J. Weiler W.D. Conce Alberto Y. Ren S. Han Huang L. Leyre A. Gramatica S. Terry R. Brad Jones Infectious Disease Division Weill Cornell Medicine New York USA Immunology and Microbial Pathogenesis Program Weill Cornell Graduate School of Medical Sciences New York NY USA.

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OP 2.3 – 00117 The EZH2 inhibitor Tazemetostat increases MHC I antigen presentation in vitro and in vivo, enhancing antiviral activities of HIV-specific CTLs

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Journal of Virus Eradication 2022年 8卷

作者： A. Gramatica A. Danesh I. Miller J. Weiler F. Khan D. Copertino U. Chukwukere L. Leyre B. Jones Division of Infectious Diseases Department of Medicine Weill Cornell Medicine New York USA Immunology and Microbial Pathogenesis Program Weill Cornell Graduate School of Medical Sciences New York USA

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Dynamic Immune Surveillance in Durable Clinical Response to Combined BTK and BCL2 Inhibition in MCL at Longitudinal Single-Cell Resolution

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BLOOD 2021年 138卷 1323-1323页

作者： Wang, Kevin Di Liberto, Maurizio Hu, Yang Huang, Xiangao Koldej, Rachel M. Ritchie, David Martin, Peter Inghirami, Giorgio Elemento, Olivier Tam, Constantine S. Chen-Kiang, Selina Columbia University Vagelos College of Physicians and Surgeons New York NY Department of Pathology and Laboratory Medicine Weill Cornell Medicine New York NY Sandra and Edward Meyer Cancer Center Weill Cornell Medicine New York NY Department of Physiology and Biophysics Weill Cornell Medicine New York NY ACRF Translational Research Laboratory The Royal Melbourne Hospital Parkville Australia Department of Medicine The University of Melbourne Parkville Australia Peter MacCallum Cancer Centre Royal Melbourne Hospital and University of Melbourne Melbourne Australia Department of Medicine Division of Hematology and Oncology Weill Cornell Medicine New York NY Graduate Program in Immunology and Microbial Pathogenesis Weill Cornell Medicine New York NY

Combined inhibition of BTK with ibrutinib and BCL2 with venetoclax is one of the most promising therapies for B cell malignancies, especially mantle cell lymphoma (MCL), where durable complete remission continued after therapy cessation in some patients ( Tam et al, NEJM 2018, Handunnetti ASH 2019 ). The MCL-intrinsic and extrinsic mechanisms underlying this deep and durable clinical response are unknown, nor have resistance mechanisms been identified. Since BTK is expressed mainly in B lineage cells and venetoclax inhibits BCL2 universally, we hypothesize that BTK inhibition selectively primes MCL cells for vulnerability to BCL2 inhibition while maintaining immune cell homeostasis, leading to differential elimination of MCL cells through immune surveillance. To test this, we undertook integrative longitudinal single-cell RNA-sequencing analysis (scRNA-seq) of PBMCs from sequential tissue and blood specimens (n=32) of 8 MCL patients before and during ibrutinib-venetoclax combination therapy, after therapy cessation or progression, as well as 4 treatment-naïve MCL patients and 4 normal subjects as controls. High dimensional analysis using a unique MCL RNA reference library that we built from bulk RNA-seq data of MCL cells from 57 patients reveals that MCL cells comprise 4 transcriptomically distinct clusters. Cluster 1 (C1) is similar to quiescent normal B cells; C2 resembles hyper-activated B cells enriched for signatures of BCR and cytokine signaling and proinflammatory pathways; C3 represents non-proliferating, long-lived MCL cells that accumulate as disease progresses; and C4 is highly proliferative, expanding with disease progression in untreated patients or on therapy. Integrative analysis of scRNA-seq and CBC with differential showed that homeostasis of all immune cells was maintained throughout ibrutinib-venetoclax therapy and after therapy cessation in 6 MCL patients with a complete response (CR). CD8+T and NK cells were functional, evidenced by the expressi

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Fungal impacts on Earth’s ecosystems

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Nature 2025年第8049期638卷 49-57页

作者： Case, Nicola T. Gurr, Sarah J. Fisher, Matthew C. Blehert, David S. Boone, Charles Casadevall, Arturo Chowdhary, Anuradha Cuomo, Christina A. Currie, Cameron R. Denning, David W. Ene, Iuliana V. Fritz-Laylin, Lillian K. Gerstein, Aleeza C. Gow, Neil A. R. Gusa, Asiya Iliev, Iliyan D. James, Timothy Y. Jin, Hailing Kahmann, Regine Klein, Bruce S. Kronstad, James W. Ost, Kyla S. Peay, Kabir G. Shapiro, Rebecca S. Sheppard, Donald C. Shlezinger, Neta Stajich, Jason E. Stukenbrock, Eva H. Taylor, John W. Wright, Gerard D. Cowen, Leah E. Heitman, Joseph Segre, Julia A. Department of Molecular Genetics University of Toronto Toronto ON Canada Biosciences University of Exeter Exeter United Kingdom University of Utrecht Utrecht Netherlands MRC Center for Global Infectious Disease Analysis Imperial College London London United Kingdom National Wildlife Health Center U.S. Geological Survey Madison WI United States Donnelly Centre University of Toronto Toronto ON Canada RIKEN Center for Sustainable Resource Science Wako Japan Department of Molecular Microbiology and Immunology Johns Hopkins University Baltimore MD United States Medical Mycology Unit Department of Microbiology Vallabhbhai Patel Chest Institute University of Delhi Delhi India National Reference Laboratory for Antimicrobial Resistance in Fungal Pathogens Vallabhbhai Patel Chest Institute University of Delhi Delhi India Department of Molecular Microbiology and Immunology Brown University Providence RI United States Department of Biochemistry and Biomedical Sciences McMaster University Hamilton ON Canada Department of Bacteriology University of Wisconsin–Madison Madison WI United States Manchester Fungal Infection Group Faculty of Biology Medicine and Health Manchester Academic Health Science Centre University of Manchester Manchester United Kingdom Fungal Heterogeneity Group Institut Pasteur Université Paris Cité Paris France Department of Biology University of Massachusetts Amherst MA United States Department of Microbiology University of Manitoba Winnipeg MB Canada Department of Statistics University of Manitoba Winnipeg MB Canada Medical Research Council Centre for Medical Mycology University of Exeter Exeter United Kingdom Department of Molecular Genetics and Microbiology Duke University Durham NC United States Joan and Sanford I. Weill Department of Medicine Weill Cornell Medicine Cornell University New York NY United States Jill Roberts Institute for Research in Inflammatory Bowel Disease Weill Cornell Medicine New York NY United St

Over the past billion years, the fungal kingdom has diversified to more than two million species, with over 95% still undescribed. Beyond the well-known macroscopic mushrooms and microscopic yeast, fungi are heterotrophs that feed on almost any organic carbon, recycling nutrients through the decay of dead plants and animals and sequestering carbon into Earth’s ecosystems. Human-directed applications of fungi extend from leavened bread, alcoholic beverages and biofuels to pharmaceuticals, including antibiotics and psychoactive compounds. Conversely, fungal infections pose risks to ecosystems ranging from crops to wildlife to humans;these risks are driven, in part, by human and animal movement, and might be accelerating with climate change. Genomic surveys are expanding our knowledge of the true biodiversity of the fungal kingdom, and genome-editing tools make it possible to imagine harnessing these organisms to fuel the bioeconomy. Here, we examine the fungal threats facing civilization and investigate opportunities to use fungi to combat these threats. © This is a U.S. Government work and not under copyright protection in the US;foreign copyright protection may apply 2025.

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