The staphylococcal toxins are responsible for a number of diseases in man and other animals. Many of them have also long been known to be powerful T cell stimulants. They do not, however, stimulate all T cells. On the contrary, each toxin reacts with human T cells bearing particular V beta sequences as part of their receptors for major histocompatibility complex protein-associated antigen. The specificity of these toxins for V beta s puts them in the recently described class of superantigens and may account for the differential sensitivity of different individuals to the toxic effects of these proteins.

These data demonstrate a smaller CD4+CD25high regulatory T-cell population in peripheral blood of individuals with early active RA prior to disease-modifying treatment. This may be a contributory factor in the susceptibility to RA and suggests novel approaches to therapy.

The proportion of peripheral blood mononuclear cells expressing the T helper cell phenotype and levels of antiendotoxin core antibody, interleukin (IL) 6 and C-reactive protein (CRP) were determined within 48 h of admission in a group of 29 patients with acute pancreatitis (16 mild, 13 severe attacks). There was a significant decrease in the proportion of T helper cells (12.2 versus 34.9 per cent, P < 0.01) and significant increases in levels of IL-6 (69.5 versus < 10 pg/ml, P < 0.01) and CRP (119 versus 30.5 mg/l, P < 0.01) in severe compared with mild attacks. During the convalescent stage at 3 months after admission, severe attacks were characterized by a significant increase in the proportion of T helper cells compared with the acute period (22.4 versus 10.6 per cent, P < 0.01). A persistently low proportion of T helper cells was associated with residual pancreatic necrosis. The presence of circulating endotoxin was demonstrated in two mild and two severe attacks using the Limulus amoebocyte lysate assay, and abnormal levels of antiendotoxin core antibodies were found in 70 and 92 per cent of mild and severe attacks respectively. There was a strong inverse correlation between levels of CRP and the proportion of T helper cells in severe disease (r = -0.76, P = 0.004). Translocation of endotoxin from the gastrointestinal tract may partly explain the abnormal levels of T helper cells, IL-6 and CRP.