Recurrent Sinopulmonary Infection and Impaired Antibody Response to Bacterial Capsular Polysaccharide Antigen in Children with Selective IgG-Subclass Deficiency

We studied 20 children with recurrent sinopulmonary infections and serum IgG levels within the normal range, who had selective IgG-subclass deficiency. Twelve of the children were IgG2 deficient, five were IgG3 deficient, and three were deficient in both IgG2 and IgG3. IgA deficiency was present in 3 of the 20 patients. In the children with IgG2 deficiency, serum antibody concentrations to the capsular polysaccharide of Hemophilus influenzae type B (Hib) were significantly lower than those in age-matched controls, both before and after immunization with the Hib capsular polysaccharide antigen, which elicits antibody predominantly of the IgG2 subclass. In contrast, their serum antibody titers to the tetanus and diphtheria toxoid protein antigens, which elicit antibody predominantly of the IgG1 subclass, were normal in comparison with those of age-matched controls. These results suggest that impairment of the antibody response to specific microbial antigens predisposes patients with selective IgG-subclass deficiencies to recurrent infections. Thus, as an aid in determining therapy, children with recurrent infections and normal total serum IgG should be evaluated for this condition. (N Engl J Med 1985; 313:1247–51.) FOUR subclasses of human IgG have been identified, each of which represents the product of a specific gene that encodes for the constant region of human immunoglobulin heavy chains. Subclasses of human IgG differ in their biologic activities. IgG1, IgG2, and IgG3 fix complement, whereas IgG4 does not. Monocytes and macrophages have detectable receptors for IgG1 and IgG3, but not for IgG2 and IgG4. IgG-antibody responses to certain classes of antigens appear to reside selectively within particular subclasses. The IgG-antibody response to polysaccharide antigens resides predominantly within the IgG2 subclass, 1 2 3 whereas the IgG-antibody response to protein antigens (e.g., tetanus and . . .