Anti-Ia monoclonal antibody (10-2.16) inhibits lymphocyte-high endothelial venule (HEV) interaction.

Lymphocyte egress from the vascular compartment into the lymph node (LN) parenchyma occurs at the postcapillary venules, termed high endothelial venules (HEVs). Lymphocyte adhesion and migration through the HEVs is a receptor-mediated, energy-dependent, process. The aim of this study was to investigate the role of MHC Class II antigen expression on lymphocyte-HEV interaction in normal (CBA) and autoimmune (MRL/l) mice.

Two distinct quinidine-induced rheumatic syndromes.

Of seven patients with quinidine-induced polyarthropathy, four had positive antinuclear antibodies and could be considered to have had quinidine-induced lupus erythematosus. The remaining three patients had milder symptoms, which occurred soon after the start of quinidine therapy, and did not have antinuclear antibodies. To confirm the association, the latter three patients were rechallenged with quinidine therapy, which caused recurrence of symptoms within 1 week.

Immunomodulators.

A new era is emerging in the therapy of rheumatic disease involving the use of biologically based immunomodulators. Cytokines, such as the interleukins and interferons, are proteins produced by activated lymphoid cells which can now be synthesised by genetic engineering techniques. These agents have already been used to correct "immune deficiencies" in patients with neoplastic and inflammatory disease e.