Second-order regulation: IFN-γ suppresses IL-17A-mediated neutrophilic inflammation
Our findings identify a distinct immunoregulatory mechanism that operates within non-lymphoid tissues, where IFN-γ limits IL-17A-mediated type 3 inflammation via STAT1. Thus, the frequent accompaniment of T <sub>H</sub> 17 cells with T <sub>H</sub> 1 cells may represent a conserved mechanism that restrains immunopathological potential of T <sub>H</sub> 17-driven neutrophilic inflammation via STAT1 signaling in non-lymphoid tissues.
Authors
- Vijay Raaj Ravi (ORCID: https://orcid.org/0000-0001-9489-1606)
- Hannah Kim (ORCID: https://orcid.org/0000-0003-2885-4377)
- Anukul T. Shenoy (ORCID: https://orcid.org/0000-0001-8861-2295)
- Olivia Harlow (ORCID: https://orcid.org/0000-0001-8142-8698)
- E. Niszczak
- Sophia H. Maxfield
- Kalyn D. Whitehead
Institutions
- University of Michigan (US)
Publication Details
- Journal
- bioRxiv (Cold Spring Harbor Laboratory)
- Published
- 2026-01-06
- DOI
- https://doi.org/10.64898/2026.01.05.697792
- Primary Topic
- Psoriasis: Treatment and Pathogenesis
- Type
- article
- Field-Weighted Citation Impact
- 0.00