Data Sheet 10_LL37-driven mast cell degranulation and inflammation in rosacea via TLR2/JAK2/STAT3 axis.zip

Introduction<p>Rosacea is a chronic inflammatory facial dermatosis with incompletely elucidated pathogenesis. LL37 is a key molecular mediator in rosacea development, and mast cells represent pivotal immune players in this process. However, the precise mechanism underlying LL37-induced mast ce...

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Päätekijä: Huiping Fan (13921872) (author)
Muut tekijät: Rui Sun (177521) (author), Qingsong Ma (21784484) (author), Xiaojin Li (152688) (author), Jiayun Liu (12651565) (author), Mogen Zhang (11152215) (author), Chen Xu (53797) (author), Dong Zhang (73558) (author), Weiyuan Ma (207735) (author)
Julkaistu: 2025
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author Huiping Fan (13921872)
author2 Rui Sun (177521)
Qingsong Ma (21784484)
Xiaojin Li (152688)
Jiayun Liu (12651565)
Mogen Zhang (11152215)
Chen Xu (53797)
Dong Zhang (73558)
Weiyuan Ma (207735)
author2_role author
author
author
author
author
author
author
author
author_facet Huiping Fan (13921872)
Rui Sun (177521)
Qingsong Ma (21784484)
Xiaojin Li (152688)
Jiayun Liu (12651565)
Mogen Zhang (11152215)
Chen Xu (53797)
Dong Zhang (73558)
Weiyuan Ma (207735)
author_role author
dc.creator.none.fl_str_mv Huiping Fan (13921872)
Rui Sun (177521)
Qingsong Ma (21784484)
Xiaojin Li (152688)
Jiayun Liu (12651565)
Mogen Zhang (11152215)
Chen Xu (53797)
Dong Zhang (73558)
Weiyuan Ma (207735)
dc.date.none.fl_str_mv 2025-11-26T05:15:10Z
dc.identifier.none.fl_str_mv 10.3389/fimmu.2025.1672021.s001
dc.relation.none.fl_str_mv https://figshare.com/articles/dataset/Data_Sheet_10_LL37-driven_mast_cell_degranulation_and_inflammation_in_rosacea_via_TLR2_JAK2_STAT3_axis_zip/30717692
dc.rights.none.fl_str_mv CC BY 4.0
info:eu-repo/semantics/openAccess
dc.subject.none.fl_str_mv Genetic Immunology
rosacea
LL37
mast cells
TLR2/JAK2/STAT3 pathway
inflammatory response
dc.title.none.fl_str_mv Data Sheet 10_LL37-driven mast cell degranulation and inflammation in rosacea via TLR2/JAK2/STAT3 axis.zip
dc.type.none.fl_str_mv Dataset
info:eu-repo/semantics/publishedVersion
dataset
description Introduction<p>Rosacea is a chronic inflammatory facial dermatosis with incompletely elucidated pathogenesis. LL37 is a key molecular mediator in rosacea development, and mast cells represent pivotal immune players in this process. However, the precise mechanism underlying LL37-induced mast cell degranulation remains undefined.</p>Methods<p>A LL37-induced rosacea-like dermatitis mouse model was established with or without ruxolitinib treatment. Hematoxylin-eosin and toluidine blue staining were used to evaluate the pathological changes. Mice skin lesions were collected for transcriptome sequencing, Western blot and immunofluorescence. In vitro, the interaction between LL37 and TLR2 on the mast cell membrane surface was detected by co-immunoprecipitation and fluorescence staining. The activation of the TLR2/MyD88/JAK2/STAT3 signaling pathway was investigated using lentivirus-mediated TLR2 knockdown, MyD88 overexpression, combined with JAK2 inhibitor (ruxolitinib). Ten patients underwent VISIA skin analysis system and severity assessment following topical ruxolitinib treatment.</p>Results<p>LL37 induces activation of the TLR2/JAK2 pathway in mast cells of rosacea-like mice. Ruxolitinib ameliorated cutaneous erythema and reduced mast cell infiltration and degranulation. In vitro experiments demonstrated that LL37 directly binds to TLR2, triggering TLR2/MyD88 pathway activation and subsequent mast cell degranulation. Mechanistically, MyD88 directly interacts with JAK2 to modulate the JAK2/STAT3 signaling axis, which governs mast cell degranulation. Topical application of ruxolitinib exhibited clinical efficacy in rosacea patients.</p>Conclusion<p>These findings collectively demonstrate that LL37 drives mast cell activation and degranulation in rosacea pathogenesis via TLR2/JAK2/STAT3 pathway activation, while ruxolitinib effectively suppresses this signaling axis. This study provides novel mechanistic insights and therapeutic strategies for rosacea management.</p>
eu_rights_str_mv openAccess
id Manara_668dd0d30e13e6a884b16a064db0acbc
identifier_str_mv 10.3389/fimmu.2025.1672021.s001
network_acronym_str Manara
network_name_str ManaraRepo
oai_identifier_str oai:figshare.com:article/30717692
publishDate 2025
repository.mail.fl_str_mv
repository.name.fl_str_mv
repository_id_str
rights_invalid_str_mv CC BY 4.0
spelling Data Sheet 10_LL37-driven mast cell degranulation and inflammation in rosacea via TLR2/JAK2/STAT3 axis.zipHuiping Fan (13921872)Rui Sun (177521)Qingsong Ma (21784484)Xiaojin Li (152688)Jiayun Liu (12651565)Mogen Zhang (11152215)Chen Xu (53797)Dong Zhang (73558)Weiyuan Ma (207735)Genetic ImmunologyrosaceaLL37mast cellsTLR2/JAK2/STAT3 pathwayinflammatory responseIntroduction<p>Rosacea is a chronic inflammatory facial dermatosis with incompletely elucidated pathogenesis. LL37 is a key molecular mediator in rosacea development, and mast cells represent pivotal immune players in this process. However, the precise mechanism underlying LL37-induced mast cell degranulation remains undefined.</p>Methods<p>A LL37-induced rosacea-like dermatitis mouse model was established with or without ruxolitinib treatment. Hematoxylin-eosin and toluidine blue staining were used to evaluate the pathological changes. Mice skin lesions were collected for transcriptome sequencing, Western blot and immunofluorescence. In vitro, the interaction between LL37 and TLR2 on the mast cell membrane surface was detected by co-immunoprecipitation and fluorescence staining. The activation of the TLR2/MyD88/JAK2/STAT3 signaling pathway was investigated using lentivirus-mediated TLR2 knockdown, MyD88 overexpression, combined with JAK2 inhibitor (ruxolitinib). Ten patients underwent VISIA skin analysis system and severity assessment following topical ruxolitinib treatment.</p>Results<p>LL37 induces activation of the TLR2/JAK2 pathway in mast cells of rosacea-like mice. Ruxolitinib ameliorated cutaneous erythema and reduced mast cell infiltration and degranulation. In vitro experiments demonstrated that LL37 directly binds to TLR2, triggering TLR2/MyD88 pathway activation and subsequent mast cell degranulation. Mechanistically, MyD88 directly interacts with JAK2 to modulate the JAK2/STAT3 signaling axis, which governs mast cell degranulation. Topical application of ruxolitinib exhibited clinical efficacy in rosacea patients.</p>Conclusion<p>These findings collectively demonstrate that LL37 drives mast cell activation and degranulation in rosacea pathogenesis via TLR2/JAK2/STAT3 pathway activation, while ruxolitinib effectively suppresses this signaling axis. This study provides novel mechanistic insights and therapeutic strategies for rosacea management.</p>2025-11-26T05:15:10ZDatasetinfo:eu-repo/semantics/publishedVersiondataset10.3389/fimmu.2025.1672021.s001https://figshare.com/articles/dataset/Data_Sheet_10_LL37-driven_mast_cell_degranulation_and_inflammation_in_rosacea_via_TLR2_JAK2_STAT3_axis_zip/30717692CC BY 4.0info:eu-repo/semantics/openAccessoai:figshare.com:article/307176922025-11-26T05:15:10Z
spellingShingle Data Sheet 10_LL37-driven mast cell degranulation and inflammation in rosacea via TLR2/JAK2/STAT3 axis.zip
Huiping Fan (13921872)
Genetic Immunology
rosacea
LL37
mast cells
TLR2/JAK2/STAT3 pathway
inflammatory response
status_str publishedVersion
title Data Sheet 10_LL37-driven mast cell degranulation and inflammation in rosacea via TLR2/JAK2/STAT3 axis.zip
title_full Data Sheet 10_LL37-driven mast cell degranulation and inflammation in rosacea via TLR2/JAK2/STAT3 axis.zip
title_fullStr Data Sheet 10_LL37-driven mast cell degranulation and inflammation in rosacea via TLR2/JAK2/STAT3 axis.zip
title_full_unstemmed Data Sheet 10_LL37-driven mast cell degranulation and inflammation in rosacea via TLR2/JAK2/STAT3 axis.zip
title_short Data Sheet 10_LL37-driven mast cell degranulation and inflammation in rosacea via TLR2/JAK2/STAT3 axis.zip
title_sort Data Sheet 10_LL37-driven mast cell degranulation and inflammation in rosacea via TLR2/JAK2/STAT3 axis.zip
topic Genetic Immunology
rosacea
LL37
mast cells
TLR2/JAK2/STAT3 pathway
inflammatory response