SUMMARYThe immune responses of 100 patients who presented with an acute idiopathic neuropathy were compared with those of age and sex matched controls. Blood lymphocytes and their subsets were counted with a fluorescent activated cell sorter. CD8 + (putative suppressor) lymphocytes were significantly reduced in the first week of the disease but total lymphocytes, total T and CD4 + (putative helper) cells were not altered. This reduction depended on the nature of the preceding infection. Serum complement C3 and C4 concentrations remained normal and immune complexes were rarely detected with a Clq binding assay. Complement-fixing antibodies to human peripheral nerve antigens were discovered in the serum of 7% of patients but only 1% of controls. Complement-fixing antibodies to galactocerebroside were not discovered in any sera. Enzymelinked immunoassays detected increased antibody responses to galactocerebroside but none at all to human P2 myelin protein in the patient sera. Forty u1 of serum from five patients injected into the sciatic nerves of rats did not induce significantly more demyelination than the serum from control patients. It is concluded that auto-immune responses can only be detected by these techniques in a small minority of patients with acute idiopathic neuropathy.The close histological resemblance between experimental allergic neuritis (EAN) and the Guillain-Barre syndrome (GBS) suggests a common auto-immune pathogenesis. The major antigen responsible for inducing EAN is a basic myelin protein, P2, MW 15000 D, which is located predominantly in the myelin of the peripheral rather than central nervous system.1-3 EAN can be transferred with lymph node cells"4 or a CD4+ T cell line.5 Cell-mediated immune mechanisms are important in pathogenesis because the development of EAN is inhibited by procedures which deplete T cells6 but antibodies to P2 can readily be detected in the blood of rats and rabbits with EAN.34 Of other myelin components which might induce an auto-immune response the most studied is galactocerebroside; rabbits immunised with this glycolipid develop a demyelinating neuropathy, lacking the perivascular lymphocyte infiltration of EAN and GBS, probably owing to complement-fixing antibodies directed against

Peritonitis in continuous ambulatory peritoneal dialysis (CAPD) patients due to S. aureus is associated with an adverse clinical outcome, suggesting impaired clearance of this organism by the host. The ability of peritoneal macrophages (PMO) derived from CAPD patients to take up S. aureus and mount a respiratory burst was investigated. Whilst significant activity was observed in the absence of opsonin, both parameters of phagocytosis were augmented by addition of 20% pooled human serum (PHS), complement-depleted PHS, and fibronectin. When used as sole opsonin, fibronectin resulted in a dose-related increase in chemiluminescent response by both blood neutrophils and PMO. The opsonic activity of dialysis effluent, as judged by neutrophil chemiluminescence, correlated with IgG and fibronectin content, but not with complement as assessed by C3 levels. The addition of urokinase to dialysate improved its opsonic properties whilst having no effect on the activity of PHS-20%; this would suggest that the formation of fibrin in dialysate, promoted by S. aureus, interferes with phagocytosis. This and the low IgG, complement and fibronectin levels in dialysate may explain in part the relatively poor clearance of this organism from the peritoneum.

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Forty four patients undergoing open heart surgery were divided into three groups. Group 1 (17 patients) underwent routine anaesthesia and surgery; group 2 (17 patients) received two doses of methylprednisolone (30 mg/kg), one during induction of anaesthesia and the other immediately before induction of cardiopulmonary bypass; and group 3 (10 patients) received pulsatile flow while undergoing pulsatile perfusion by the heart-lung machine. A modification of the previously described technique was used to detect and measure complement activation in plasma before and during the bypass period using crossed immunoelectrophoresis.About 45% of all patients showed measurable complement activation (>455%) during cardiopulmonary by-

Ten isolates of coagulase-negative staphylococci, collected from patients receiving treatment with continuous ambulatory peritoneal dialysis (CAPD), exhibited marked differences in the degree of opsonisation when incubated in 10% and 1% pooled human serum, 10% and 1% heat-treated serum, Hanks’ Balanced Salt Solution, and timed peritoneal dialysis (PD) effluent. The addition of exogenous IgG to PD effluent results in a greater increase in opsonisation in those fluids with the weakest inherent opsonic activity, but is ineffective against the majority of isolates in the absence of heat-Iabile opsonic activity. The results of this in vitro study suggest that host resistance to CAPD peritonitis due to coagulasenegative staphylococci may be determined as much by the characteristics of the contaminating strain, as by the opsonising activity of PD effluent.