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The mononuclear cells from. the joint fluid of certain patients with inflammatory arthritis are shown to be more cytotoxic to a polyploid strain of homologous liver cells than were equivalent numbers of peripheral blood lymphocytes From the same donors. The diagnostic categories of these patients are essentially similar to those of a group of patients studied by Hedberg (1967) in whom joint fluid mononuclear cells were cytotoxic to monolayers of human foetal fibroblasts. Evidence is presented to show that this cytotoxic activity is attributable to lymphocytes, as opposed to polymorphonuclear leucocytes or phagocytic mononuclear cells which adhere to glass. It is not excluded that the latter population may also have some cytotoxic potential. It is argued that the target cell damage described in this paper is probably not induced by any antigen on the target cell. The implications of this suggestion are discussed in relation to the pathogenesis of inflammatory joint disease. [ABSTRACT FROM AUTHOR]

The article presents information on rheumatoid factors reacting with autologous native γG--globulin and joint fluid γG aggregates. Inflammatory joint fluids from patients with definite or classical rheumatoid arthritis (RA), selected because they precipitated strongly with rheumatoid factors (RF), were examined by sucrose density gradient ultra-centrifugation for sedimentation of γG-globulin (γG) and behavior of RF activity. It has been shown that in patients with a very low ratio between RF activity in joint fluid and serum, the joint fluid often precipitates with RF isolated from high titred rheumatoid sera. In two patients with classical RA it was further evident that the precipitate was formed by reaction of RF with aggregated γG present in the joint fluid.