Shahnaz Begum, Md Jamil Hossain, Insun Kim, Hyun Su Min, Yu Na Lim, Hyun-Jeong Cho, Jin-Hyeob Ryu
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引用次数: 0
Abstract
Background: Alopecia areata (AA) are hair loss disorders with distinct pathogenetic mechanisms involving immune dysregulation and microRNA modulation. AA, a T cell-mediated autoimmune disease, is characterized by sudden hair loss, with interferon-gamma (IFN-γ) playing a pivotal role in pathogenesis. The upregulation of IFN response genes, including IFN-inducible chemokines CXCL9, CXCL10, and CXCL11, in lesional skin reflects the activation of the IFN response pathway and contributes to immune cell recruitment and inflammation.
Results: Recent research highlights the role of SIRT1, a class III histone deacetylase, in modulating immune responses in AA. SIRT1 inhibition promotes the production of Th1 cytokines and chemokines, impairing inflammation, while SIRT1 activation suppresses autoreactive responses through NF-κB deacetylation and STAT3 phosphorylation. Additionally, antisense oligonucleotides (ASOs) targeting miR-485-3p show therapeutic potential in promoting hair regrowth and mitigating inflammation in murine models of androgenic alopecia (AGA) and AA.
Conclusion: Understanding chemokine dysregulation provides key insights into AA pathogenesis and highlights TAMI-M as a potential therapy for reducing inflammation and promoting hair regeneration. These findings advance the exploration of immune, microRNA, and SIRT1 pathways as targets for novel hair loss treatments.
期刊介绍:
BMC Immunology is an open access journal publishing original peer-reviewed research articles in molecular, cellular, tissue-level, organismal, functional, and developmental aspects of the immune system as well as clinical studies and animal models of human diseases.