Good news! Soon arthritis will be history! However, this is early stage research.
"... The foundational finding is hoped to direct research toward entirely new pathways to treat this autoimmune disease affecting millions. ...
The new lab-based research focused on a type of human cell called synovial fibroblasts. These are the cells that line joints, and in cases of rheumatoid arthritis, inflammation in synovial fibroblasts is triggered by TNF-alpha.
In looking for a protein that plays a role in joint inflammation the researchers homed in on a molecule called sulfatase‑2. Prior cancer studies have indicated sulfatase‑2 plays a role in tumor growth, and it's known to be involved in immune cell signaling processes. ...
Excitingly, the experiments revealed significantly reduced inflammatory responses in the cells when sulfatase‑2 was removed. ... “This tells us that TNF‑alpha relies on sulfatase‑2 to drive inflammation ...
It’s important to note this research is still in very early stages. These findings are so far only established in cell models and further animal studies will be needed to validate these mechanisms before any kind of human treatment can be considered. ...
And there is other ongoing work looking at blocking sulfatase‑2 to treat cancers. In fact, a sulfatase‑2 inhibitor is already in Phase 2 human clinical trials as a treatment for severe forms of brain cancer ..."
Excitingly, the experiments revealed significantly reduced inflammatory responses in the cells when sulfatase‑2 was removed. ... “This tells us that TNF‑alpha relies on sulfatase‑2 to drive inflammation ...
It’s important to note this research is still in very early stages. These findings are so far only established in cell models and further animal studies will be needed to validate these mechanisms before any kind of human treatment can be considered. ...
And there is other ongoing work looking at blocking sulfatase‑2 to treat cancers. In fact, a sulfatase‑2 inhibitor is already in Phase 2 human clinical trials as a treatment for severe forms of brain cancer ..."
"Scientists have identified a protein known as sulfatase‑2 that plays a critical role in the damage caused by rheumatoid arthritis. ..."
From the abstract:
"Extracellular sulfatase-2 (Sulf-2) influences receptor–ligand binding and subsequent signaling by chemokines and growth factors, yet Sulf-2 remains unexplored in inflammatory cytokine signaling in the context of rheumatoid arthritis (RA). In the present study, we characterized Sulf-2 expression in RA and investigated its potential role in TNF-α-induced synovial inflammation using primary human RA synovial fibroblasts (RASFs). Sulf-2 expression was significantly higher in serum and synovial tissues from patients with RA and in synovium and serum from hTNFtg mice. RNA sequencing analysis of TNF-α-stimulated RASFs showed that Sulf-2 siRNA modulated ~2500 genes compared to scrambled siRNA. Ingenuity Pathway Analysis of RNA sequencing data identified Sulf-2 as a primary target in fibroblasts and macrophages in RA. Western blot, ELISA, and qRT‒PCR analyses confirmed that Sulf-2 knockdown reduced the TNF-α-induced expression of ICAM1, VCAM1, CAD11, PDPN, CCL5, CX3CL1, CXCL10, and CXCL11. Signaling studies identified the protein kinase C-delta (PKCδ) and c-Jun N-terminal kinase (JNK) pathways as key in the TNF-α-mediated induction of proteins related to cellular adhesion and invasion. Knockdown of Sulf-2 abrogated TNF-α-induced RASF proliferation. Sulf-2 knockdown with siRNA and inhibition by OKN-007 suppressed the TNF-α-induced phosphorylation of PKCδ and JNK, thereby suppressing the nuclear translocation and DNA binding activity of the transcription factors AP-1 and NF-κBp65 in human RASFs. ..."
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