ArticleImmunity2024
CXCL16-dependent scavenging of oxidized lipids by islet macrophages promotes differentiation of pathogenic CD8
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Article in Immunity, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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24citing papers in PubMed
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Who cites it
24 citing papers in PubMed.
- ACT001 suppresses ox-LDL-mediated macrophage ferroptosis via activating the NRF2 pathway: AnExperimental and therapeutic medicine · 2026Article
- Donor macrophage depletion permits posttransplant tolerance induction in a murine islet transplant model.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2026Article
- Iron, Copper, and Zinc Dyshomeostasis in Cardiovascular and Cerebrovascular Diseases: Redox Mechanisms, Evidence Levels, and Translational Prospects.International journal of molecular sciences · 2026Review
- Ferroptotic propagation: from single-cell execution to tissue-scale death programs.Cell research · 2026Review
- Bioelectric Reawakening by a Self-Powered Thermoelectric Hydrogel Accelerates Diabetic Ulcer Repair.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Immune context governs stage-specific responses to depleting anti-PD-1 antibody in type 1 diabetes.Cell biomaterials · 2026Article
- Targeting GPR34 in damage-associated macrophages enhances anti-tumor immunity and the efficacy of Surufatinib in pancreatic cancer.Signal transduction and targeted therapy · 2026Article
- Loss of Bone Marrow β1/β2-Adrenergic Receptors Reprograms Host-Microbiota Interactions and Protects Against Diet-Induced Obesity.bioRxiv : the preprint server for biology · 2026Article
- From damage signals to immune modulators: oxidized lipids in immunometabolic inflammation.Journal of lipid research · 2026Review
- Ferroptosis: unveiling a transformative perspective in the landscape of autoimmune diseases.Frontiers in immunology · 2026Review
- A microenvironment-driven HLA-II-associated insulin neoantigen elicits persistent memory T cell activation in diabetes.Nature immunology · 2026Article
- Neoepitopes at the crossroads of immunometabolism: metabolic remodeling of antigen presentation in type 1 diabetes.Frontiers in immunology · 2026Review
- The role of pancreatic islet macrophages in type 2 diabetes mellitus: from underlying pathological mechanisms to therapeutic target discovery.Metabolism open · 2025Review
- Islet Tissue Macrophages in Immunity Homeostasis and Type 1 Diabetes.Clinical reviews in allergy & immunology · 2025Review
- Integrative analysis identifies shared therapeutic pathways in thyroid eye disease and diabetes mellitus.Scientific reports · 2025Article
- Tissue Resident and Infiltrating Immune Cells: Their Influence on the Demise of Beta Cells in Type 1 Diabetes.Biomolecules · 2025Review
- Immunocyte lipid metabolic reprogramming: a novel pathway for targeted intervention in autoimmune diseases.Frontiers in immunology · 2025Review
- Mini review: Interleukin-32 as a key mediator of type 1 diabetes pathogenesis.Frontiers in immunology · 2025Review
- Interactions between islet-resident macrophages and β cells in diabetes.Frontiers in immunology · 2025Review
- Macrophage-derived chemokines in T cell regulation: implications for cancer immunotherapy.Frontiers in immunology · 2025Review
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Authors and funding
16 authors.
Neetu SrivastavaDepartment of Pathology and Immunology, Division of Immunobiology, Washington University School of Medicine, St. Louis, MO, USA; The Andrew M. and Jane M. Bursky Center for Human Immunology and Immunotherapy Programs, Washington University School of Medicine, St. Louis, MO, USA.
Hao HuDepartment of Pathology and Immunology, Division of Immunobiology, Washington University School of Medicine, St. Louis, MO, USA; The Andrew M. and Jane M. Bursky Center for Human Immunology and Immunotherapy Programs, Washington University School of Medicine, St. Louis, MO, USA.
Orion J PetersonDepartment of Pathology and Immunology, Division of Immunobiology, Washington University School of Medicine, St. Louis, MO, USA; The Andrew M. and Jane M. Bursky Center for Human Immunology and Immunotherapy Programs, Washington University School of Medicine, St. Louis, MO, USA.
Anthony N VomundDepartment of Pathology and Immunology, Division of Immunobiology, Washington University School of Medicine, St. Louis, MO, USA; The Andrew M. and Jane M. Bursky Center for Human Immunology and Immunotherapy Programs, Washington University School of Medicine, St. Louis, MO, USA.
Marta StremskaDepartment of Pathology and Immunology, Division of Immunobiology, Washington University School of Medicine, St. Louis, MO, USA.
Mohammad ZamanDepartment of Pathology and Immunology, Division of Immunobiology, Washington University School of Medicine, St. Louis, MO, USA; The Andrew M. and Jane M. Bursky Center for Human Immunology and Immunotherapy Programs, Washington University School of Medicine, St. Louis, MO, USA.
Shilpi GiriDepartment of Pathology and Immunology, Division of Immunobiology, Washington University School of Medicine, St. Louis, MO, USA; The Andrew M. and Jane M. Bursky Center for Human Immunology and Immunotherapy Programs, Washington University School of Medicine, St. Louis, MO, USA.
Tiandao LiDepartment of Developmental Biology, Center of Regenerative Medicine, Washington University School of Medicine, St. Louis, MO, USA.
Cheryl F LichtiDepartment of Pathology and Immunology, Division of Immunobiology, Washington University School of Medicine, St. Louis, MO, USA; The Andrew M. and Jane M. Bursky Center for Human Immunology and Immunotherapy Programs, Washington University School of Medicine, St. Louis, MO, USA.
Pavel N ZakharovDepartment of Pathology and Immunology, Division of Immunobiology, Washington University School of Medicine, St. Louis, MO, USA.
Bo ZhangDepartment of Developmental Biology, Center of Regenerative Medicine, Washington University School of Medicine, St. Louis, MO, USA.
Nada A AbumradCenter for Human Nutrition, Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA; Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, MO, USA.
Yi-Guang ChenDepartment of Pediatrics, Medical College of Wisconsin, Milwaukee, WI, USA.
Kodi S RavichandranDepartment of Pathology and Immunology, Division of Immunobiology, Washington University School of Medicine, St. Louis, MO, USA; VIB/UGent Inflammation Research Centre and Biomedical Molecular Biology, Ghent University, Ghent, Belgium.
Emil R UnanueDepartment of Pathology and Immunology, Division of Immunobiology, Washington University School of Medicine, St. Louis, MO, USA; The Andrew M. and Jane M. Bursky Center for Human Immunology and Immunotherapy Programs, Washington University School of Medicine, St. Louis, MO, USA.
Xiaoxiao WanDepartment of Pathology and Immunology, Division of Immunobiology, Washington University School of Medicine, St. Louis, MO, USA; The Andrew M. and Jane M. Bursky Center for Human Immunology and Immunotherapy Programs, Washington University School of Medicine, St. Louis, MO, USA. Electronic address: wanx@wustl.edu.
Funding
Washington University Nutrition Obesity Research CenterP30DK056341 · NIDDK · WASHINGTON UNIVERSITY · PI Dominic N Reeds · 1999 to 2026
$30.2MWU P&FP30DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI Clay F. Semenkovich · 2013 to 2026
$27.1MWashington University Rheumatic DiseasesResearch Resource-based CenterP30AR073752 · NIAMS · WASHINGTON UNIVERSITY · PI Alfred Hyoungju Kim · 2018 to 2026
$7.6MThe role of beta-cell crinophagy in generating diabetogenic neoepitopesR01DK134437 · NIDDK · WASHINGTON UNIVERSITY · PI Xiaoxiao Wan · 2023 to 2026
$2.4MAutoimmune Diabetes: Macrophage ResponsesR01AI162591 · NIAID · WASHINGTON UNIVERSITY · PI Xiaoxiao Wan · 2022 to 2026
$2.3MNIAID NIH HHS R01 AI162591NIAMS NIH HHS P30 AR073752NIDDK NIH HHS P30 DK020579NIDDK NIH HHS P30 DK056341NIDDK NIH HHS R01 DK134437
Abstract
The pancreatic islet microenvironment is highly oxidative, rendering β cells vulnerable to autoinflammatory insults. Here, we examined the role of islet resident macrophages in the autoimmune attack that initiates type 1 diabetes. Islet macrophages highly expressed CXCL16, a chemokine and scavenger receptor for oxidized low-density lipoproteins (OxLDLs), regardless of autoimmune predisposition. Deletion of Cxcl16 in nonobese diabetic (NOD) mice suppressed the development of autoimmune diabetes. Mechanistically, Cxcl16 deficiency impaired clearance of OxLDL by islet macrophages, leading to OxLDL accumulation in pancreatic islets and a substantial reduction in intra-islet transitory (Tex
Indexed as
AutoimmunityCD8-Positive T-LymphocytesCell DifferentiationChemokine CXCL16Diabetes Mellitus, Type 1Islets of LangerhansLipoproteins, LDLMacrophagesMice, Inbred NODMice, KnockoutAnimalsMiceMice, Inbred C57BLChemokine CXCL16Cxcl16 protein, mouseLipoproteins, LDLoxidized low density lipoproteinautoimmunityCD8 T cell differentiationCD8 T cell exhaustionCD8 T cell ferroptosisCXCL16oxidized LDLpancreatic isletsPD-1 checkpoint blockadetissue-resident macrophagestype 1 diabetes
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.