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A radioimmunometric method was developed for the quantification of lactoferrin molecules natively bound to blood monocyte and lymphocyte surfaces and the estimation of the surface lactoferrin-binding capacity of these cells after their incubation with exogenous lactoferrin. Values of surface lactoferrin obtained were greatest for monocyte-rich isolates (9,168 +/- 1,713 molecules/cell; n = 19). The values of monocyte surface lactoferrin for males were similar to those of premenopausal females (8,980 +/- 2,378 (n = 8) and 9,427 +/- 2,606 molecules/cell (n = 11), respectively), but males had slightly lower values of monocyte surface lactoferrin binding capacity than did premenopausal females (10,447 +/- 2,478 molecules/cell versus 15,958 +/- 3,731 molecules/cell, respectively; p > 0.05). Expressed as saturation of the monocyte surface lactoferrin binding capacity, values of 97.2% +/- 22.6% for males and 76.6% +/- 14.3% for females were calculated. Intermediate values of surface lactoferrin were found in B-lymphocyte-rich isolates from five patients with B-cell chronic lymphocytic leukemia. In T-lymphocyte-rich preparations, there were low levels of native lactoferrin expression (154 +/- 63 molecules of lactoferrin/cell; 3 isolates). The present technique should permit additional quantitative studies of mononuclear cell surface lactoferrin to determine the role of lactoferrin surface binding and analyses of factors that modulate this binding.

Several therapeutic agents currently are used to treat rheumatoid arthritis (RA). However, there is no compelling evidence that any of these agents substantially alters the long-term destructive course of RA. Advances in biotechnology have led to a better understanding of mechanisms that underlie autoimmune diseases such as RA. Although the etiology of RA remains unknown, there now is considerable insight regarding the immune and inflammatory pathways that ultimately lead to cartilage and bone destruction. Therapies with monoclonal antibodies directed against cell surface constituents, fusion toxins against cell activation markers, and cytokine inhibitors all have been shown to be safe and possibly efficacious in early open trials in RA. They now are being more rigorously tested in double-blind, placebo-controlled trials. Early experience with these biologic agents in humans, as well as data obtained from the use of these agents in animal models of autoimmune disease, are reviewed. In addition, experimental studies with "blocking peptides" and immunization with autoreactive T cell receptor peptides will be reviewed, and implications for therapy in RA will be discussed.