Lupus & antiphospholipid syndrome
Modifying T cell phenotypes using TYK2 inhibitor and its implications for the treatment of systemic lupus erythematosus
Authors' conclusion
Tfh1 cells can induce T-bet+ B cell production and may contribute to SLE pathogenesis-associated processes. TYK2 inhibitor may fine-tune the immune imbalance by suppressing Tfh1 differentiation and maintaining Treg cell differentiation, thereby preserving IL-2 signalling, unlike other JAK inhibitors.
Study context
- Population
- Untreated patients with systemic lupus erythematosus (SLE) and healthy controls; human peripheral blood samples
- Comparison
- Untreated SLE patients vs healthy controls; JAK inhibitors vs TYK2 inhibitors in vitro
Main finding
As reported in the abstract
- Tfh1 cell numbers increased in peripheral blood of patients; activated T regulatory (Treg) cell counts decreased relative to Tfh1 cell counts
- T follicular helper (Tfh)/Treg imbalance remarkably pronounced in LN, especially types III and IV active nephritis
- Tfh1 cell infiltration in LN tissues (immunohistochemistry)
- Tfh1 cells co-cultured with naïve B cells elicited greater induction of T-bet+ B cells than controls
- IL-12-induced STAT1/4 phosphorylation and Tfh1 differentiation inhibited by both JAK and TYK2 inhibitors
- IL-2-induced STAT5 phosphorylation and IL-2+TGFβ-induced Treg differentiation inhibited by JAK inhibitors but not by TYK2 inhibitors
Original publication
Modifying T cell phenotypes using TYK2 inhibitor and its implications for the treatment of systemic lupus erythematosus. RMD Open. Published 13 June 2024. doi:10.
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