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  • Title: Abnormal haemoglobins in the Sudan savanna of Nigeria. II. Immunological response to malaria in normals and subjects with sickle cell trait.
    Author: Cornille-Brøgger R, Fleming AF, Kagan I, Matsushima T, Molineaux L.
    Journal: Ann Trop Med Parasitol; 1979 Apr; 73(2):173-83. PubMed ID: 386969.
    Abstract:
    Children born in areas hyperendemic for Plasmodium falciparum are protected by maternal antibodies for up to about five months of life, after which they are subject to intense infection until they acquire sufficient immunity--by about five years of age. Children with sickle cell trait (Hb.AS) are at an advantage during these critical years, probably because of preferential phagocytosis of parasitized red cells. This could lead to either (i) early processing of antigen by macrophages and an accelerated immune response, or (ii) less antigenic stimulus and hence lower antibody production. Immunoglobulin (Ig)G and IgM determinations, agar gel diffusion (Ouchterlony) against soluble P. falciparum antigen, the indirect fluorescent antibody (IFA) test using P. falciparum and P. malariae antigens, and the indirect haemagglutination (IHA) test with P. falciparum antigen were performed on sera from a population with different Hb electrophoretic types in the hyperendemic malarial area of Garki, Kano State, Nigeria. Plasma immunoglobulins and antimalarial antibodies rose with age. After the first year of life, lower mean concentrations of immunoglobulins (especially IgM), and lower mean titres of antibodies specific against P. falciparum (Ouchterlony, IHA and less significantly IFA) were present in Hb.AS compared to Hb.AA; these differences increased with age. Antimalarial intervention was followed by a decline of all values and final levels showed little difference between haemoglobin types. It was unlikely that either a relative inability to produce antibody or a more rapid catabolism of immunoglobulins was responsible for the lower levels in sickle cell trait. The observations are more easily explained by the hypothesis that Hb.AS persons have less antigenic stimulus due to the early removal of parasitized sickled cells by macrophages, which then degrade the antigens. The antibody difference between Hb.AA and Hb.AS increased throughout life, suggesting that this process remained a feature of sickle cell trait even after parasite frequencies and densities were similar in the two Hb groups. These observations have implications in the aetiology of tropical splenomegaly syndrome, which is rarely seen in sickle cell trait subjects. Mean IgG and IgM were slightly higher in Hb.AS than Hb.AA infants, the difference for IgG achieving significance. This suggested that during infancy early phagocytosis of parasitized cells had led to enhanced processing of antigen and hence an earlier immune response in Hb.AS, but this was unlikely to be a major factor in survival. IFA titres against P. malariae were slightly but not significantly lower in Hb.AS, possibly as a result of cross-reaction with P. falciparum antibody or of a slight degree of protection against P. malariae.
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