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The lymphocyte transformation test was used to evaluate the cellular immune response in 31 adult patients with MCNS in comparison with 30 normal control and 49 patient (CRF, FSGN, MGN) control groups. The results showed that the stimulation indices of the lymphocytes in MCNS group were significantly lower than those of the normal control and patient control groups with the exception of CRF group. In cross studies, lymphocytes obtained from normal individuals were incubated in homologous serum obtained from MCNS patients in relapse, and lymphocytes from MCNS patients in relapse were incubated in normal homologous AB serum. In both circumstances there was a depressed lymphocyte function which indicates that there is a defect in lymphocyte itself as well as a serum inhibitory factor(s) during the active stage of the MCNS. This depressed cellular immune response returned to normal level during remission of the patients with MCNS.

One hundred and seven patients with acute viral hepatitis (AVH) were studied prospectively regarding the viral aetiological agent HAV, HBV and NANB (by exclusion) using radioimmunoassay. Acute HAV infection occurred in 43 patients, and acute HBV infection in 34 patients, while HDS occurred in two patients only. Acute, presumably NANB, infection occurred in 28 patients. Ten out of 28 sera of patients with AHBV infection were positive for smooth muscle antibody by immunofluorescence. Important findings include: (1) presence of delta superinfection in the absence of HBsAg; (2) HBsAg as the only marker in two patients with AHBV infection; (3) concurrent presence of HBsAg and anti-HBsAg in three patients with AHBV infection.

Most patients with pulmonary tuberculosis have impaired T-lymphocyte function as measured by dinitrochlorobenzene (DNCB) sensitization and response to tetanus toxoid. The humoral immune response as gauged by the ability to respond to typhoid vaccine was not affected. Tuberculous patients had higher immunoglobulin levels than normal controls. The relative proportions of T lymphocytes in patients were lower than in controls while those of B lymphocytes were normal. By these criteria, rifampin treatment did not seem to cause immunosuppression.

Peripheral blood mononuclear cells from altogether 45 nickel-sensitive patients and 37 controls were assayed for various T and B cell variables. All the patients, but none of the controls, fulfilled our in vitro criteria for a positive response to nickel sulphate (NiSO4). We report normal T and B lymphocyte counts, normal spontaneous plaque-forming cell (PFC) numbers, normal serum immunoglobulin levels, and no demonstrable specific cytotoxic T lymphocyte activity associated with nickel sensitivity. We could detect only a slight increase in the number of PFC and in the number of cytoplasmic immunoglobulin positive (cIg+) cells following stimulation of the patients' cells with NiSO4 for 6 days in culture. Apart from a transient increase in the [3H]thymidine uptake by patients' cells stimulated with NiSO4 in vitro, and a transient drop in the OKT4/OKT8 ratio, there were no major differences in the values of the above variables before and after in vivo challenge of 3 patients with NiSO4. Blood from only 2 of the latter 3 patients was tested in the DNA synthesis test. We conclude that apart from the DNA synthesis test, none of these tests is of any use as an aid to diagnosis in patients with nickel sensitivity. A careful attitude towards patch testing should be maintained.