Lupus & antiphospholipid syndrome
Semaphorin 5A promotes Th17 differentiation via PI3K-Akt-mTOR in systemic lupus erythematosus
Authors' conclusion
These findings demonstrated that Sema5A-PlexinA1 axis acts as a key mediator on Th17 differentiation
Study context
- Population
- Systemic lupus erythematosus (SLE) patients and healthy controls (HC); Peripheral blood mononuclear cells (PBMCs) and CD4+ T cells
- Comparison
- SLE patients vs healthy controls; Sema5A treatment and PlexinA1 knockdown in CD4+ T cells
- Outcome
- Role of Sema5A in promoting Th17 cell differentiation in SLE
Methodological detailsin vitro, Enzyme Linked Immunosorbent Assay (ELISA), quantitative RT-PCR (qRT-PCR), Western Blot, flow cytometry, recombinant human Sema5A (rhSema5A) treatment and small interfering RNA (siRNA) knockdown
- In vitro
- ELISA, qRT-PCR, Western Blot, flow cytometry
- rhSema5A treatment and siRNA knockdown
Main finding
As reported in the abstract
- IL-17A elevated in SLE patients and positively correlated with Sema5A
- PlexinA1 upregulated and mainly expressed in CD4+ T cells of SLE
- Sema5A treatment induced Th17 differentiation, did not affect Th1 and Th2 skewing
- Associated with upregulation of RORγt by Th17 cells, not T-bet or GATA3 in Th1 and Th2 cells
- PlexinA1 knockdown regulates IL-17A production by CD4+ T cells
- Sema5A-PlexinA1 axis promoted Th17 differentiation via PI3K/Akt/mTOR signalling
Original publication
Semaphorin 5A promotes Th17 differentiation via PI3K-Akt-mTOR in systemic lupus erythematosus. Arthritis Res Ther. Published 19 November 2024. doi:10.
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