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Cross‐Reactivity of Monospecific Anti‐HL‐A Antisera 1
Author(s) -
Mittal Kamal K.
Publication year - 1975
Publication title -
vox sanguinis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.68
H-Index - 83
eISSN - 1423-0410
pISSN - 0042-9007
DOI - 10.1111/j.1423-0410.1975.tb00588.x
Subject(s) - antigen , antiserum , platelet , cross reactivity , antibody , microbiology and biotechnology , cross reactions , chemistry , homologous chromosome , in vitro , reactivity (psychology) , immunology , biology , biochemistry , medicine , pathology , gene , alternative medicine
. 32 ‘monospecific’ anti‐HL‐A alloantisera were absorbed in separate tests with platelets from a maximum of 56 different persons and examined for residual cytotoxicity against target lymphocytes from one or two unrelated persons having the homologous (or test) antigen. Of the 799 combinations in which platelets had the test antigen, 715 (90%) were specifically inhibited; of the 720 combinations in which platelets had the cross‐reactive antigen(s) (but not the test antigen), 417 (58%) were specifically cross‐inhibited; and of the 1,839 combinations in which platelets had neither the homologous nor a discernable cross‐reactive antigen, 133 (7%) were cross‐inhibited ‘nonspecifically’. Earlier findings of cross‐reactivity were confirmed, and results suggested that HL‐A1, HL‐A10 and W30 on platelets may cross‐inhibit anti‐HL‐A2 antibodies; HL‐A7 and W21 may cross‐inhibit anti‐HL‐A5 and anti‐W5 antibodies; W16 may cross‐inhibit anti‐HL‐A5 antibodies; and W22 may cross‐inhibit anti‐HL‐A13 antibodies.