Rheumatoid Arthritis Mice

RA models include spontaneous models (K/BxN serum transfer, collagen-induced arthritis), gene-targeted models (knockout or knockin of RA susceptibility genes), and conditional models (tissue specific deletion of genes involved in RA pathogenesis). Selection depends on research question, timeline, and specific mechanisms of interest.

Common Cre drivers include CD4-Cre (T lymphocytes), LysM-Cre (macrophages and neutrophils), CD11c-Cre (dendritic cells), and CX3CR1-Cre (monocytes/macrophages). Selection depends on whether you're studying T-cell contributions, macrophage function, or combined immune mechanisms in RA.

RA phenotyping includes clinical assessment (paw swelling, arthritis score, joint inflammation), histological analysis (synovial inflammation, cartilage damage, bone erosion, pannus formation), serum biomarkers (rheumatoid factor, anti-CCP antibodies, inflammatory cytokines), and functional assessment (grip strength, mobility).

Yes. Genetic modifications can be combined with environmental factors (collagen immunization, serum transfer, adjuvant) to model gene-environment interactions in RA. Conditional approaches enable study of how specific genes contribute to RA pathogenesis in controlled challenge protocols.