Multiple cell lineages contribute to the pathogenesis of inflammatory arthritis independent of antibodies. Murine studies implicate multiple lymphocyte subtypes in specific contexts, including CD4⁺ T cells, exFoxP3-converted Tregs, entheseal-resident T cells, and γδ T cells. CD8⁺ T cells and B cells/plasma cells are abundant in synovium but their role is unclear. Evidence for the presence and function of synovial T_RM cells is preliminary. Fibroblasts within the synovium are heterogeneous and contribute via mediator production and direct attachment and invasion, including into cartilage. Myeloid cells of multiple types participate actively in disease. Neutrophils appear essential for the normal evolution of chronic inflammatory arthritis in most contexts. Local resident macrophages, recruited monocytes, and newly differentiated macrophages are implicated both in propagation and in resolution of synovitis. Mast cells can initiate arthritis and are abundant in chronic synovitis, but their role in established arthritis is not well defined. Osteoclasts mediate bone erosion and can potentially amplify or even initiate joint inflammation. Downstream effector pathways include cytokines (e.g., TNF, IL-1, IL-6, IL-8, IL-17), chemokines such as ligands for the chemokine receptors CCR1 and CXCR2, lipid mediators such as leukotriene B₄, proteases, and direct tissue injury. Illustrated by Mao Miyamoto.