Review · PMID 41848778
Pathophysiological aspects of primary Sjogren's disease: From epithelial activation to systemic autoimmunity — VialBase Research
Sjogren's disease involves epithelial dysregulation, innate immune activation, and adaptive immune response
Last updated · 2026 · Ritter J, Dorner T · Z Rheumatol
Key findings
- Sjogren's disease involves epithelial dysregulation, innate immune activation, and adaptive immune response
- TLR and IFN blockade, CD154/CD40 blockade, B-cell depletion emerging as therapeutic approaches
- Tuftsin-based peptides (Selank's parent) relevant to immune modulation in autoimmune contexts
- IL-6 pathway central to SjD pathogenesis -- Selank modulates IL-6
Sjogren’s Disease Immunopathology and Selank Relevance (PMID: 41848778)
Context
While this paper does not directly study Selank, it characterizes the immune pathways (IL-6, innate immune activation, T-B cell interaction) that Selank modulates through its tuftsin-derived mechanism.
Key Pathways Relevant to Selank
- IL-6 dysregulation: Central to SjD chronic inflammation — Selank modulates IL-6 production
- Innate immune activation: Tuftsin (Selank’s parent peptide) stimulates macrophage/neutrophil activity
- Type I IFN signature: Prominent in SjD; Selank’s gene expression effects touch interferon pathways
Relevance
Provides theoretical basis for Selank investigation in autoimmune conditions where IL-6 and innate immune dysregulation are central, such as Sjogren’s disease.
See Also
- Parent compound: Selank