ReviewFrontiers in immunology2026
Macrophage polarization in Sjögren's syndrome: from mechanisms to therapeutic translation.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sjögren's syndrome (SS) is a chronic systemic autoimmune disease characterized by damage to exocrine glands, and no effective treatment is currently available to reverse glandular fibrosis. As core effector cells of innate immunity, macrophages play a pivotal role in the dynamic imbalance of polarization states, which critically influences inflammation initiation, tissue injury, and irreversible fibrosis in SS. This review systematically delineates the heterogeneity of M1/M2 macrophage subsets, their spatiotemporal dynamics, and their functional transitions across different pathological stages of SS: M1 predominance drives early pro-inflammatory damage, M1/M2 interplay sustains chronic inflammation in the middle stage, and aberrant M2 polarization promotes late-stage glandular fibrosis. We further dissect the multi-level regulatory network underlying macrophage polarization imbalance, including immune cell crosstalk, core signaling pathways, non-coding RNA epigenetic regulation, and immunometabolic reprogramming. The in-depth mechanisms by which M2 macrophages drive the progression of glandular fibrosis are also summarized. In this context, we describe how certain traditional Chinese medicine (TCM) formulas and monomeric compounds can effectively restore the balance of macrophage polarization by targeting relevant pathways and molecular nodes. Moreover, we analyze the major bottlenecks currently hindering the clinical translation of macrophage-targeted strategies and propose innovative approaches, including tissue-specific delivery, spatiotemporally tailored modulation, integrated TCM-western medicine therapy, biomarker-guided patient stratification, and early-window intervention. Finally, we discuss the potential of cutting-edge technologies such as single-cell multi-omics, spatial transcriptomics, gene editing, and organoid models to decode the heterogeneity of macrophage subsets and their interactions with the microenvironment. Integration of these multidisciplinary tools will facilitate the development of safe, effective, and personalized therapeutic strategies targeting macrophage polarization for SS.
Indexed as
Identifiers
What Socratic holds
Registered trials
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 Socratic graph.