Characterization of Dendritic Cells and Myeloid-Derived Suppressor Cells Expressing Major Histocompatibility Complex Class II in Secondary Lymphoid Organs in Systemic Lupus Erythematosus-Prone Mice DOI Open Access

F Uribe,

F. J. González-Martínez,

Sebastián A. Echeverría-Araya

и другие.

International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(24), С. 13604 - 13604

Опубликована: Дек. 19, 2024

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by self-antibody production and widespread inflammation affecting various body tissues. This driven the breakdown of immune tolerance, which promotes activation autoreactive B T cells. A key feature SLE dysregulation in antigen presentation, where antigen-presenting cells (APCs) play a central role perpetuating responses. Dendritic (DCs) are highly specialized for presentation among APCs. At same time, myeloid-derived suppressor (MDSCs) can also express MHC-II molecules, although their less understood. Utilizing model, MRL/MpJ-Faslpr/J, we determined presence different phenotypes DCs MDSCs expressing secondary lymphoid organs, along with gene expression ICOSL, CD80 CD86 spleen. Our study that most abundant population APCs organs corresponds to cDC CD103−CD11b+ MHC-II+ throughout development. Additionally, ICOSL increased over becoming more preponderant week 16 could indicate it crucial pathway development progression pathology. In 16, observed positive correlation between M-MDSC IFN-γ-producing CD4+

Язык: Английский

Human and Murine Toll-like Receptor-Driven Disease in Systemic Lupus Erythematosus DOI Open Access
Susannah von Hofsten, Kristin Andreassen Fenton, Hege Lynum Pedersen

и другие.

International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(10), С. 5351 - 5351

Опубликована: Май 14, 2024

The pathogenesis of systemic lupus erythematosus (SLE) is linked to the differential roles toll-like receptors (TLRs), particularly TLR7, TLR8, and TLR9. TLR7 overexpression or gene duplication, as seen with Y-linked autoimmune accelerator (Yaa) locus agonist imiquimod, correlates increased SLE severity, specific polymorphisms gain-of-function variants are associated enhanced susceptibility severity. In addition, X-chromosome location its escape from inactivation provide a genetic basis for female predominance in SLE. absence TLR8 TLR9 have been shown exacerbate detrimental effects leading upregulated activity disease severity mouse models regulatory functions proposed involve competition endosomal trafficking chaperone UNC93B1. However, recent evidence implies more direct, on activity. association between age-associated B cells (ABCs) autoantibody production positions these potential targets treatment SLE, but lack markers necessitates further research precise therapeutic intervention. Therapeutically, targeting TLRs promising strategy treatment, drugs like hydroxychloroquine already clinical use.

Язык: Английский

Процитировано

8

Animal models of autoimmunity: a relentless pursuit of accurate pre-clinical models DOI Creative Commons
Laurence Morel

Autoimmunity, Год журнала: 2025, Номер 58(1)

Опубликована: Фев. 5, 2025

Язык: Английский

Процитировано

1

Drug repurposing for glomerular diseases: an underutilized resource DOI
Monica Suet Ying Ng, Gursimran Kaur, Ross S. Francis

и другие.

Nature Reviews Nephrology, Год журнала: 2024, Номер 20(11), С. 707 - 721

Опубликована: Июль 31, 2024

Язык: Английский

Процитировано

6

Progress in the field of animal models of antiphospholipid syndrome DOI Creative Commons
Xinnan Gao, Dan Ma,

Liangyu Mi

и другие.

Autoimmunity, Год журнала: 2024, Номер 57(1)

Опубликована: Авг. 18, 2024

Antiphospholipid syndrome (APS) is an autoimmune disease characterized by recurrent arteriovenous thrombosis and pathological pregnancy, accompanied persistent antiphospholipid antibodies, (aPL). The incidence of APS increasing year year, clinicians lack understanding this type disease, easy to misdiagnose miss the diagnosis. Therefore, it extremely important establish a suitable animal model reduce process development as much possible improve clinicians' understanding. This review will summarize models from aspects modeling methods, mechanism, evaluation indicators advantages disadvantages providing reference for finding highly similar human APS, helping researchers further clarify pathogenesis find potential therapeutic targets, so achieve early diagnosis, intervention, ultimately prognosis patients.

Язык: Английский

Процитировано

1

Plasma exosomes may mediate the development of lupus nephritis in patients with systemic lupus erythematosus DOI
Jie Liu,

Yuanju Liu,

Yinde Xu

и другие.

Lupus, Год журнала: 2024, Номер unknown

Опубликована: Окт. 31, 2024

Background Lupus nephritis (LN) is the most serious complication of systemic lupus erythematosus (SLE), and plasma exosomes may serve as a bridge. MicroRNAs (miRNAs) are abundant in exosomes, so this study aimed to explore role exosome-derived miRNA development LN. Methods The publicly available data containing exosomal miRNAs SLE patients healthy controls were researched, differential expression functional enrichment analysis was conducted. Then, from extracted, accuracy preliminarily verified. PKH26 dye used label detect whether can enter HK2 cells. Evaluation impact on cell viability done by utilizing CCK-8 assay. Flow cytometry measure apoptosis. Results Plasma successfully extracted identified. Through pulbilic subsequent qPCR validation, we observed that miR-20b-5p overexpressed patients, whereas miR-181a-2-3p downregulated. Then revealed these primarily regulate processes such apoptosis, autophagy, inflammation. flow conducted after co-incubation peripheral blood mononuclear cells confirmed indeed And without affecting activity. In addition, promote apoptosis autophagy. Overexpression could inhibit upregulate bcl2, beclin1. At same time, trend towards increased rates miR-20b-5p, although difference did not reach statistical significance. enhance caspase3 becin1 while suppressing bcl2 LC3β. Conclusion Our research indicates presence depletion mediate promotion autophagy cells, thereby causing kidney damage

Язык: Английский

Процитировано

0

Characterization of Dendritic Cells and Myeloid-Derived Suppressor Cells Expressing Major Histocompatibility Complex Class II in Secondary Lymphoid Organs in Systemic Lupus Erythematosus-Prone Mice DOI Open Access

F Uribe,

F. J. González-Martínez,

Sebastián A. Echeverría-Araya

и другие.

International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(24), С. 13604 - 13604

Опубликована: Дек. 19, 2024

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by self-antibody production and widespread inflammation affecting various body tissues. This driven the breakdown of immune tolerance, which promotes activation autoreactive B T cells. A key feature SLE dysregulation in antigen presentation, where antigen-presenting cells (APCs) play a central role perpetuating responses. Dendritic (DCs) are highly specialized for presentation among APCs. At same time, myeloid-derived suppressor (MDSCs) can also express MHC-II molecules, although their less understood. Utilizing model, MRL/MpJ-Faslpr/J, we determined presence different phenotypes DCs MDSCs expressing secondary lymphoid organs, along with gene expression ICOSL, CD80 CD86 spleen. Our study that most abundant population APCs organs corresponds to cDC CD103−CD11b+ MHC-II+ throughout development. Additionally, ICOSL increased over becoming more preponderant week 16 could indicate it crucial pathway development progression pathology. In 16, observed positive correlation between M-MDSC IFN-γ-producing CD4+

Язык: Английский

Процитировано

0