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The cytotoxic effect of normal human blood lymphocytes on Chang cells in tissue culture was investigated. Cell damage was measured by release of 51Cr from pre-labelled tissue culture ‘target’ cells. This method was sensitive and rendered highly reproducible results. Released 51Cr was not re-utilized. About 25 per cent of the 51Cr was spontaneously released from labelled Chang cells when incubated for 24 hours at 37°. Lymphocytes at a lymphocyte/Chang cell ratio of 25:1 led to a slight increase of this release. When phytohaemagglutinin was also present, about 50—60 per cent of the isotope appeared in the medium. Under these conditions target cells were significantly damaged -within 1 hour. At a lymphocyte/Chang cell ratio of only 1:1, weak cytotoxic effects were also noted after 24 hours of incubation. The results of dose—response experiments suggested that a considerable proportion of the lymphocytes participated in the reaction. Individual variation of the cytotoxic effect of lymphocytes from different donors suggested that it could be related to the degree of histoincompatibility between lymphocytes and Chang cells. Under the present conditions contaminating erythrocytes or granulocytes did not interfere with the cytotoxic action of the lymphocytes.

Sera from patients with Plasmodium falciparum, P. vivax or P. ovale malaria were selected according to their high levels of antibodies against human erythrocyle membranes as measured in a microELISA. The specificity of the anti-erythrocyte antibodies in these sera and two normal sera was investigated by means of an immunoblotting technique in combination with SDS-polyacrylamide gel electrophoresis. All the patients' sera as well as the control sera contained antibodies against several erythrocyte polypeptides. As compared with normal sera, most malaria sera showed elevated levels of antibodies against polypeptides of 80K, 70K, 40K and 28K molecular weights. Two sera reacted strongly against a polypeptide with an electrophoretic mobility similar to the α subunit of spectrin. One serum showed strong reaction and several other sera, including normal sera, showed weak reaction against a 45K molecular weight polypeptide corresponding to actin. No pervading differences were seen in the pattern of specificities of the anti-erythrocyte ghost antibodies between sera from patients with P. falciparum, P. vivax or P. ovale infections. [ABSTRACT FROM AUTHOR]

Blood lymphocytes from thirteen patients with CLL were studied for surface-bound Ig (SIg), Fc receptors (EA rosettes), receptors for sheep erythrocytes (E rosettes) and receptors for Helix pomatia A haemagglutinin (FTP), a carbohydrate-binding protein with specificity for N-acetyl-D- galactosamine and related sugars. Fluorescein-labelled HP binds to subpopulations of human peripheral blood lymphocytes (PBL) treated with neuraminidase. In normal peripheral blood, HP binds to the T-lymphocytes while the majority of the B cells bearing surface-bound immunoglobulin do not have receptors for HP. In untreated CLL, HP binds to 90-100% of the neur-aminidase-treated PBL. Almost all of the SIg-positive cells in CLL patients also have receptors for HP. Two groups of patients were found: in one the total fraction of SIg+ cells was ⩽50% and about 30% of these lost their Ig during incubation at 37° C. No such loss of Slig was revealed in the remaining patients where total SIg+fraction was ≈70%. These patients usually had higher blood lymphocyte counts, probably reflecting a more advanced disease. CLL patients in remission with low numbers of leukaemic cells also had low numbers of blood lymphocytes carrying both SIg and HP-receptors. It is concluded that leukaemic cells carry both HP receptors and SIg. Testing of this combination therefore provides a valuable new tool for monitoring patients with CLL. [ABSTRACT FROM AUTHOR]

Isotypes (IgM and IgG-1 to 4) of anti-P. falciparum antibodies were investigated in sera of malarial patients or immune donors by enzyme linked immunosorbent assay (ELISA) and two indirect immunofluorescence assays (IFAs), one staining intra-erythrocytic parasites of all stages and the other a restricted number of parasite antigens deposited in the membrane of infected erythrocytes by invading merozoitcs (Perlmann & Wahlgren, 1983; Perlmann et al., 1984, Wahlgren et al., 1985 a). There was no correlation in overall antibody titre between the two IKAs. Antibodies of both IgM and all tour IgG isotypes were detected in both assays. With the IFA for intracellular parasites a brilliant fluorescence was obtained with antibodies of all isotypes. However IgG-2 antibodies often gave staining restricted to the surface of schizonts. The incidence and reactivity in individual sera of antibodies of the different isotypes did not relate to the immune status of the donors (acute infection or clinically immune) but related well to the degree of malarial exposure as reflected by the overall antibody titres. This, in all three assays, high titred sera frequently contained antibodies of all isotypes white low titred sera usually only contained antibodies of IgM, IgG-1 and IgG-3 isotype. On average, the overall expression of antibodies of different isotypes in individual sera appears to reflect a sequential downstream (5' to 3') activation of the corresponding Igh-C genes in P. falciparum specific B cell clones. [ABSTRACT FROM AUTHOR]