All joints were sectioned in the plane of the fore paw. (A and B) Representative joint sections from unchallenged Fib⁺ and Fib^– mice. (C–H) Representative joint sections from CII-immunized Fib⁺ and Fib^– mice harvested at day 40 and stained with hematoxylin and eosin. CIA-challenged Fib⁺ mice generally exhibited severe joint pathology, with individuals occasionally displaying obliterated joint architecture (C) and granulation tissue invading into the underlying trabecular bone. The metacarpophalangeal joints from Fib⁺ mice often displayed significant cartilage and bone erosion (E, arrowheads) with robust inflammatory infiltrates and synovial hyperplasia (G, arrows). Asterisk in C denotes pannus tissue. Joints from CII-immunized Fib^– mice typically displayed far less overall joint space damage with only mild synovial inflammation and hyperplasia (D and F, arrows). Many metacarpophalangeal joints from CIA-challenged Fib^– mice were nearly free of microscopically apparent disease (H). (I–L) Immunohistochemical stain of fibrin(ogen) within joints of unchallenged and CII-immunized mice harvested 40 days after primary CII immunization. No fibrin deposition was observed within joints from unchallenged Fib⁺ mice (I). However, robust fibrin staining (brown, denoted by asterisk) was observed within inflamed and hyperplastic synovial tissue (J) and on articular surfaces (K, arrows) in Fib⁺ mice. As expected, no fibrin(ogen) was detectable within joint sections prepared from CII-immunized Fib^– mice (L) regardless of the degree of joint damage. Scale bar: 100 μm.