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Changes of T and B lymphocyte populations have been studied in chronic active hepatitis and liver cirrhosis. It was found that E rosette-forming T lymphocyte counts were significantly lower in this group of diseases than in the controls. The B cell count did no change significantly as compared to the controls. Incubation with levamisole was followed by a significant increase in active E rosette-forming and total T-cell counts. The authors have appraised the experimental results by comparison to published findings.

Decreased activity of T-suppressor cells plays an important role in the pathogenesis of lupus erythematosus disseminatus. The authors investigated the in vitro effect of levamisole on the histamine inhibited E-rosette forming T-lymphocyte subpopulation in patients affected by LED and in healthy persons. Histamine significantly inhibited the E-rosette forming T-lymphocyte subpopulation in the patient group as compared to controls. This effect of histamine could be reversed by levamisole. It may be anticipated that the E-rosette forming T-cell subpopulation which can be inhibited by histamine is identical to histamine-receptor carrying T-lymphocyte subpopulation with suppressor properties. The possible mechanisms of histamine induced inhibition of E-rosette forming T-cells has been discussed on the basis of literary data.

The effect of alcohol ingestion on the prognosis of chronic liver diseases was studied'n. Among 880 patients with chronic liver diseases the percentage of alcoholics was high, 33%, compared to 3.2% in the control group. The period of survival time is decreased by one half in patients with regular alcohol ingestion. According to 'in vitro' investigations they report that in chronic active hepatitis the low Et-rosette forming cell number is further decreased after incubation with alcohol, and ethanol inhibits the immune-stimulating effects of levamisole on Ett-rosette forming cells.

Fibronectin was detected by immunofluorescence on the surface of one fraction of separated normal peripheral blood lymphocytes using FITC-conjugated anti-human fibronectin antibodies. Approximately one fifth of isolated B cells and 7% of O cells contained surface bound fibronectin but T cells failed to stain. There were no detectable free receptors for fibronectin on the surfaces of the lymphocytes in the different subsets isolated from healthy controls as studied using FITC-labelled purified fibronectin. The per cent of B and O cells bearing surface bound fibronectin was markedly decreased in patients with acute and chronic lymphocytic leukemias and non Hodgkin's lymphoma, only 1-4% of B and 1-2% of O cells stained with FITC-labelled antifibronectin immunoglobulins. FITC-conjugated fibronectin was not bound to the different lymphoblasts isolated from patients with leukemia and lymphoma. Treatment of cells with trypsin and EDTA removed fibronectin bound to the cell surfaces. Fibronectin attached to the surfaces of lymphocytes may have an immunoregulatory function.

Peripheral blood lymphocytes and the "in vitro' changes of the T-cell count after levamisole treatment were studied in twenty-two patients with systemic lupus erythematosus and in eighteen normal controls using E-rosette assay to quantify T-cells and EAC-assay to quantify B-lymphocytes. T-cell count was significantly lower in the patient group compared with the control group. B-cell numbers did not change significantly. The decrease of the T-cell count was accompanied by an increase of the null-cell number in patient groups. The levamisole treatment "in vitro' produced an increase in the active-T and total T-lymphocyte counts and led to the decrease of null-cell numbers. These data confirm the available evidence that levamisole "in vitro' may induce the maturation of immature T-lymphocytes in SLE.

Isolated and washed cryoimmunoglobulins from 15 patients were studied for the presence of fibronectin by immunodiffusion tests. Two of the isolated cryoglobulins proved to the pure monoclonal immunoglobulins (IgGl kappa and IgGl lambda), nine contained both monoclonal IgM kappa and polyclonal IgG and four were composed of polyclonal IgG, IgM and IgA by immunoelectrophoresis. Double immunodiffusion analysis detected the presence of fibronectin in each of the separated cryoimmunoglobulins. In a solid phase radioimmunoassay, I125 labelled purified fibronectin proved to bind to isolated human monoclonal myeloma proteins of IgGl kappa and IgG3 lambda subclasses. Fibronectin seems to be present not only in mixed polyclonal but also in mixed monoclonal-polyclonal and in monocomponent cryoimmunoglobulins, and it may be bound to one of the immunoglobulin components of the cryoglobulins.