Antibodies directed to capsular
polysaccharides form an essential component in the defence against
infections with encapsulated bacteria such as Streptococcus pneumoniae and Haemophilus influenzae type b. Immune responses to
polysaccharide antigens can occur in the absence of a functional thymus and the
antigens are therefore designated as thymus independent. However, regulatory T cells may influence the magnitude of the antibody response to capsular
polysaccharide antigens. So-called thymus independent type 2
antigens share several features of their immune response such as late development of antibody synthesis in ontogeny, no memory formation and a restricted isotype (
IgM,
IgG2) and idiotype usage. In infants and young children up to the age of 2 years the antibody response to capsular
polysaccharides is inadequate resulting in an increased incidence of diseases such as
pneumonia,
meningitis,
otitis and other forms of bacteremic disease. Anti-capsular
polysaccharide antibody deficiency does occur in a number of well defined immunodeficiency syndromes including hypo- or agammaglobulinaemia, selective
IgA and/or
IgG subclass deficiency,
Wiskott-Aldrich syndrome,
DiGeorge anomaly and also in acquired immune deficiencies such as
AIDS, and some forms of lymphoid
malignancies. In elderly and in conditions such as
splenectomy an increased incidence of
infections with encapsulated bacteria does occur, sometimes but not always on basis of a defect in antibody formation. Clinicians are often confronted with young patients older than 2 years of age suffering from recurrent severe
bacterial infections of the respiratory tract. In these patients no overt immunodeficiency is demonstrable but recent results indicated that a small percentage may show a selective defect in the antibody response since upon vaccination with
polysaccharide vaccines no increase in antibody titer does occur. Though
antibodies to
polysaccharide antigens in young children are mainly of the
IgM and
IgG1 (
IgG3) isotype, in older children and adults the
polysaccharide antibodies are predominantly localized in the
IgG2 subclass. The bridge between
IgG2 type
antibodies and phagocytosis of encapsulated bacteria is constituted by
Fc gamma receptors for
IgG2 on effector cells. The recent finding that allotypes of
Fc gamma RIIa do exist that either bind or do not bind
IgG2 type
antibodies strongly suggests that the defence of a given individual to encapsulated bacteria apart from an intact antibody formation and the
complement system also is determined by the allotype of the appropriate
Fc gamma receptor.(ABSTRACT TRUNCATED AT 400 WORDS)