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The effect of blood transfusions on the immune response of 46 thalassaemic children was studied. Cell-mediated immune response was evaluated by performing skin tests to specific (streptokinase-streptodornase and candidin) and nonspecific (dinitrochlorobenzene and phytohaemagglutinin) antigens. Antibody response to a specific antigen (tetanus toxoid) was estimated by measuring the tetanus antitoxin titre before and after vaccination. No gross impairment of cell-mediated immunity was elicited. The larger proportion of negative phytohaemagglutinin skin tests found in thalassaemic patients does not necessarily suggest a cell-mediated immunity impairment, since this skin reaction is also affected by other factors, especially the inflammatory skin response. The transfused antibodies may inhibit the recipient’s sensitization and primary immune response to the homologous antigen, especially when the antibody level in the transfused blood is high, whereas the secondary immune response is not affected.

Sera from 530 children suffering from various diseases and from 64 controls were tested for smooth muscle autoantibodies (SMA) by indirect immunofluorescence. A high incidence of SMA (51-86%) was found in patients with viral and bacterial infections (viral hepatitis, infectious mononucleosis, measles, mumps, chickenpox, typhoid fever, and brucellosis), independently of liver invovlvement, and in patients with acute haemolytic anaemia due to G-6-PD deficiency (48%). By contrast, the incidence of SMA from patients with beta-thalassaemia major and idiopathic thrombocytopenic purpura was no higher than in the controls. The discrepancy in incidence in haemolytic anaemias due to different causes may reflect the effect of endogenous and extrinsic agents. In the viral infections, SMA were mainly of the IgM class and gave an 'SMA-V' staining pattern. In bacterial infections (typhoid fever and brucellosis), SMA were either IgG only or IgM and IgG, and the staining pattern was also mainly 'SMA-V'. In infections which affect or may affect the liver (viral hepatitis, infectious mononucleosis, typhoid fever, and brucellosis), SMA was present at high titres (1:80-1:320), whereas in infections not affecting the liver (measles, mumps, and chickenpox) the titres were lower (less than or equal to 1:80). In most patients SMA occurred transiently and without apparent pathogenetic significance. The antigen against which infection-induced SMA is directed is not actin; its nature has yet to be identified.

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