Inflammatory arthritis is characterized by pathogenic fibroblast like synoviocyte (pFLS) overgrowth in the synovium. pFLS can directly degrade cartilage through pannus formation. pFLS also secrete cytokines including IL-6 and CCL2/MCP-1, which in turn are likely to promote M1 or inflammatory macrophage/monocytes. Resident synovial macrophages (RSMs) likewise secrete IL-1B and TNF-a, which promote FLS secretion of IL-6 and CCL2. Understanding how these two major cell types of the synovium communicate to create pro-inflammatory or anti-inflammatory environments is key to preventing or attenuating inflammatory arthritis. This project aims to individually and sequentially block RSM or FLS signaling in an inflammatory environment to uncover the initiation and perpetuation mechanisms of arthritis.

Publications

Cyndari KI, Scorza BM, Zacharias ZR, Pessôa-Pereira D, Strand L, Mahachi K, Oviedo JM, Gibbs L, Butler KL, Ausdal G, Hendricks D, Yahashiri R, Elkins JM, Gulbrandsen T, Peterson AR, Willey MC, Fairfax KC, Petersen CA. Resident synovial macrophages in synovial fluid: Implications for immunoregulation. Clin Immunol. 2025 Feb;271:110422. doi: 10.1016/j.clim.2024.110422. Epub 2024 Dec 17. PMID: 39701169.

Honors/Awards

AAI 2025 poster presenter Graduate Student Senate Travel Award winner 2025