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Various immunological parameters exploring both T- and B-cell functions were determined in a group of 74 symptom-free Italian haemophiliacs treated with commercial concentrate imported from the USA and were correlated with the presence in their serum of antibody to HTLV-III. There was a strong correlation between HTLV-III seropositivity and the amount of concentrate consumed. A significant correlation between HTLV-III seropositivity and T-cell alterations, such as T4/T8 ratio less than 1 and reduction in the absolute number of T4+ lymphocytes, or B-cell alterations such as hypergammaglobulinaemia and enhanced spontaneous IgG synthesis in vitro, was also observed.

A significant reduction in the proportion and absolute number of circulating T gamma (suppressor) lymphocytes was observed in 15 adult patients with idiopathic thrombocytopenic purpura (ITP). The proportion of T gamma cells was also reduced in the spleen of four patients so investigated. This abnormality was not seen in 5 patients cured by splenectomy whilst it persisted in 3 who remained thrombocytopenic after splenectomy. The proportion of Tmu (helper) lymphocytes in ITP was normal. These findings, similar to those reported in systemic lupus erythematosus, suggest that an inbalance of the immunoregulatory T-cell subsets may be important in the pathogenesis of ITP.

A significant increase in the proportion (mean 38% +/- 9.3 SD) and absolute number of T gamma (suppressor) lymphocytes was observed in 13 patients with chronic lymphocytic leukaemia (CLL) compared with 20 normal controls (mean 19% +/- 6.5). Conversely, the proportion of T mu (helper) lymphocytes was lower in CLL (mean 27% +/- 9.3) than in the controls (mean 40% +/- 4), although the absolute numbers were normal or increased. It is suggested that an imbalance of T-lymphocyte subsets controlling B-lymphocyte differentiation may be relevant in the pathogenesis of CLL or some of its associated features.

Studies of platelet survival time, ‘turnover’, sequestration with use of 51Cr-labelled platelets as well as platelet size distribution as an index of the age of platelet population and the rate of platelet production were performed in 13 patients with cyanotic congenital heart disease (CCHD). Platelet survival was significantly shorter in CCHD than in the normal subjects. The platelet population was younger in CCHD and the size distribution of platelets showed a shift to the right, i.e. the percentage proportion of megathrombocytes was increased (24–52 %) as compared with controls (6–15 %). The absolute number of megathrombocytes was also increased in some patients. The differences from the control values were statistically significant. The results suggested that an increased peripheral destruction of platelets (thrombocytolytic state) is present in children with CCHD.

Inbred albino rats, aged 5–6 months, were given a single injection of Cortisol or injections of Cortisol every 6 h for up to 3 d. At varying times in relation to the Cortisol administration a single injection of 3H-thymidine was given. The eosinophils in the peripheral blood and in suspensions of splenic tissue were studied by counting the absolute number of eosinophils and by autoradiography. These investigations showed that Cortisol induces a sharp decrease of eosinophils in the splenic tissue due primarily to a reduction in the number of mature eosinophils. At the same time, there was a relative increase in the number of proliferating eosinophils. Long-term administration of Cortisol results in an inhibiton of mitotic activity of the eosinophil precursors. There was no indication that the peripheral eosinopenia following Cortisol administration could be due to migration of eosinophils to the spleen and/or splenic destruction of eosinophils.