Findings position exosomes as central contributors to HT pathogenesis and highlight their value as emerging diagnostic biomarkers and targets for innovative immunotherapeutic strategies.
This review compares how EVs remodel the immune microenvironment in HT, type 2 diabetes mellitus (T2DM), and related disease contexts, with attention to donor cells, cargo, recipient pathways, biomarkers, and therapeutic implications.
Yao Ma, Wei-Na Jiang, Tong Zhou et al.· Frontiers in Immunology· 0 citations
A testable positive-feedback perspective in which thyrocyte ERS injury and immune effector amplification may mutually reinforce one another is proposed, in which thyrocyte ERS injury and immune effector amplification may mutually reinforce one another.
X. Si, Zhi-Xun Guo, Ge-Na Jiao et al.· Frontiers in Immunology· 0 citations
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...
Keying Zhu, Ximao Li, Qian-Lei Xu et al.· Frontiers in Immunology· 0 citations
The growing body of evidence suggests a complicated association between papillary thyroid cancer (PTC) and Hashimoto’s thyroiditis (HT). Although HT is a major risk factor for PTC development, it is also associated with improved patient outcomes. However, the molecular mechanisms between these two diseases remain uncle...
Xin Lin, Zhi Chen, Dan-Dan Song et al.· Frontiers in Endocrinology· 0 citations
Goflikicept effectively normalized dysregulated immune responses in IRP, supporting the broader therapeutic potential of IL-1 blockade in NLRP3-mediated inflammatory diseases.
A. Golovkin, E. Markelova, E. Ignatieva et al.· Inflammation Research· 0 citations
This study provides a multimodal characterization of necroptosis in HT, showing that the inflammatory immune microenvironment is associated with TFC loss and activation of an RIPK3-MLKL-predominant necroptosis-related program, without detectable upregulation of total or phosphorylated RIPK1.
Dong-Yu Yang, Cihang Lu, Wei-Ping Teng et al.· Frontiers in Immunology· 0 citations
We use cookies to run the site and, with your consent, for analytics and to show ads.
See our Cookie Policy.