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HL‐A Linked Genetic Control of Immune Response in Man

After the original observation by Gorer & Schiitze (1938) that some breeds of mice were more susceptible to particular infections than other breeds, research in this field has given many arguments for genetic control of immune response to a variety of antigens in animals (McDevitt & Benacerraf 1969). In several instances this control has been shown to be linked to loci controlling histocompatibility antigens in mouse, guinea pig or rat (Benacerraf 1974, McDevitt et al. 1974a, McDevitt & Bodmer 1974). This article presents the preliminary results of a study of immune response in human twins. If a pair of sibs is HL-A identical and if the genetic control of immune response is associated with loci located on the same chromosome carrying the loci responsible for HL-A antigens, one can expect a greater similarity in immune response than in a pair of sibs which is not HL-A identical. Thus, greater homogeneity in immune response in HL-A identical sibs is considered an argument in favour of linkage between some immune response locus and the HL-A loci. For the first part of our study we chose antibody titres to antigens in vaccines or common infectants as parameters for antibody response in man. There are reports on associations between immune response and particular HL-A haplotypes, but these are not informative in choosing an antigen for linkage studies (Jersild et al. 1973, Levine et al. 1972). Antibody responses to poliomyelitis virus and diphtheria toxoid were chosen because they are included in routinely administrated vaccinations of children in the Nether-