{"doi":"10.3389/fcell.2024.1383642","title":"Editorial: Role of innate and adaptive immune cells in the metabolic syndrome","abstract":"Ray and Odum et al. delve deeper into the role of macrophages as regulators of inflammation. They emphasize that diverse macrophage subsets have unique functions in both promoting and resolving inflammation. In this regard, the authors highlight that embryonicallyderived resident macrophages and infiltrated monocyte-derived macrophages have distinct and contrasting roles in regulating chronic inflammation. They elaborately review a large body of literature that clarifies our mechanistic understanding of how macrophages exert pro-and antiinflammatory effects in the context of four chronic diseases -insulin resistance and adipose tissue inflammation, atherosclerosis, non-alcoholic fatty liver disease and neurodegeneration. These factors can be broadly categorized into shared mechanisms related to lipid handling, production of cytokines and lipid mediators, efferocytosis or phagocytosis, and microRNAmediated gene regulation. These pathways are promising targets for therapy. The authors further cautioned against the blocking of pathways that are active in both pro-and anti-inflammatory macrophage subsets, such as CCR2-CCL2 driven cell recruitment, as this will also impair resolution and tissue repair.George et al. explore the mechanisms that allow the pleiotropic cytokine, IFN-g, to both promote and restrain inflammation in the context of type 1 diabetes. As an inflammatory mediator, IFN-g induces apoptosis and cell death, promotes expression of chemokines, receptors and adhesion molecules that facilitate immune cell recruitment and infiltration, augments antigen presentation and autoreactive T cell activation. On the other hand, IFN-g has anti-inflammatory effects by limiting the proliferation of pathogenic T cells and by upregulating immune checkpoint molecules in the target tissue. The authors discuss that the pro-inflammatory role of IFN-g is mediated by the activation of the Janus kinase/signal transducer and activator of the transcription (JAK/STAT) signaling pathway, while the regulatory effect is due to inhibition of JAK/STAT signaling by SOCS1 (suppressors of cytokine signaling 1). Based on this, the authors advocate the use of JAK inhibitors as strategies to limit inflammation in type 1 diabetes.Liu et al. further extend this possibility and describe the importance of the JAK/STAT signaling pathway in the context of diabetic kidney disease (DKD), the most important microvascular complication of diabetes. The authors extensively reviewed available literature and proposed that JAK/STAT activation can affect the pathogenesis of DKD by influencing multiple factors, including the renin-angiotensin system (RAS), fibrosis, immune cell-mediated inflammation, cellular senescence, autophagy, and epithelial-to-mesenchymal transition (EMT). As these mechanisms are interconnected, inhibition of JAK/STAT signaling can limit disease progression by blocking multiple pathways. Finally, the authors discuss the potential of specific inhibitor molecules, natural compounds and other drugs that target the JAK/STAT pathway, as prospective treatment options in DKD. The safety and efficacy of one of these drugs, Baricitinib, in treating DKD patients, has been explored in a phase II, multicenter, double-blind, randomized, controlled clinical trial.Guo et al. focus on upstream activators of signaling pathways and shed light on the role of pattern-recognition receptors (PRRs) in orchestrating maladaptive inflammation in endometriosis, a gynecological disorder that is characterized by hormonal imbalance and abnormal growth outside the uterine cavity. Recent studies have shown a pivotal role of immune cells in the etiology of endometriosis. The authors suggest that an inflammatory endometrial microenvironment is maintained by interactions between PRRs on immune cells with pathogenand damage-associated molecular patterns (PAMPs and DAMPs) in the surrounding milieu. They discuss the potential involvement of all five major groups of PRRs, namely the tol","journal":"Frontiers in Cell and Developmental Biology","year":2024,"id":494564,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":0,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9459,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2024-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":324393,"name":"Holger Winkels","orcid":"0000-0003-1333-2031","position":1,"is_corresponding":false},{"id":324394,"name":"Marco Orecchioni","orcid":"0000-0002-3602-8510","position":2,"is_corresponding":false},{"id":567478,"name":"Estefanía Quesada‐Masachs","orcid":"0000-0001-6033-1176","position":3,"is_corresponding":false},{"id":535206,"name":"Thomas Riffelmacher","orcid":"0000-0002-0372-5272","position":4,"is_corresponding":false},{"id":490438,"name":"Payel Roy","orcid":"0000-0003-2511-068X","position":0,"is_corresponding":true}],"reference_count":3,"raw_metadata":null,"created_at":"2026-07-19T02:09:11.736910Z","pmid":"38455074","pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}