We have developed a mixed passive haemagglutination test for the detection of
platelet antibodies. This test is essentially a combination of a modified test of mixed agglutination
and reversed passive haemagglutination. Using this test, platelet allo-antibodies
(HLA antibodies and non-HLA antibodies) were found to be detected with very high sensitivity
in the sera of pregnant women and transfused patients. The platelet crossmatch test
was performed for patients who had to receive massive platelet transfusion. There was a good
correlation between the result of the crossmatch and clinical platelet recovery.
These results suggest that the observed decreased in PLT aggregation after storage can improve in the body after transfusion, and transfused PLTs have similar aggregation ability compared to the PLTs derived from the patient.
Mixed passive hemagglutination (MPHA) test was established using platelet-supernatant and indicator cells coated with purified antihuman IgG antibodies. The supernatant was shown to contain HLA A and B antigens, platelet alloantigens and blood group A, B and H antigens released spontaneously from the platelets. Unlike the MPHA with platelet monolayer, the in vitro-formed immune complex (IC) or IC containing pathologic sera did not give positive reactions in the MPHA with platelet supernatants presumably due to relatively low Fc receptor activities of the supernatants. By means of this test, HLA A or B antibodies were demonstrated in sera of 32 (44%) of 72 patients with multiple platelet transfusions including ‘cytotoxicity negative absorption positive’ sera. This test would provide a sensitive procedure for cross-match of sera of recipients of platelet transfusion and screening of HLA A and B typing sera.
Abstract. We have developed a mixed passive haemagglutination test for the detection of platelet antibodies. This test is essentially a combination of a modified test of mixed agglutination and reversed passive haemagglutination. Using this test, platelet allo‐antibodies (HLA antibodies and non‐HLA antibodies) were found to be detected with very high sensitivity in the sera of pregnant women and transfused patients. The platelet crossmatch test was performed for patients who had to receive massive platelet transfusion. There was a good correlation between the result of the crossmatch and clinical platelet recovery.
We studied immunological functions of peripheral blood lymphocytes (PBL) from human T-cell leukemia virus type I (HTLV-I)-seropositive healthy carriers in vitro. Proliferative responses of PBL to T-cell and B-cell mitogens such as concanavalin A (Con A), pokeweed mitogen (PWM), and Staphylococcus aureus Cowan I (SAC) were moderately impaired in HTLV-I carriers compared with normal controls. Immunoglobulin (Ig)-producing activity of PBL stimulated with B-cell mitogens were also impaired in HTLV-I carriers. However, cytotoxic T-cell activity induced by in vitro culture was not impaired but slightly increased in HTLV-I carriers. Natural killer-cell activity was only slightly decreased. By a flow cytofluorometric analysis of the cell surface phenotypes of PBL, the percentage and the mean fluorescence intensity (MFI) of CD 3-positive cells and CD 4-positive cells were significantly decreased in HTLV-I carriers. The percentage and the MFI of CD 8-positive cells was not changed. The percentage and the MFI of CD 25-positive cells were increased. These results suggest that some immunological abnormalities are already present in HTLV-I carriers and such abnormalities have some roles for the leukemogenesis from the infection of the HTLV-I into adult T-cell leukemia (ATL).
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