INTESTINAL AND CIRCULATING ANTIBODY-FORMING-CELLS IN IGA-DEFICIENT INDIVIDUALS AFTER ORAL CHOLERA VACCINATION

In search for a possible explanation for the different susceptibility to mucosal infections in IgA-deficient (IgAd) individuals, the frequen cy of total immunoglobulin-secreting cells (ISC) and vaccine-specific antibody-secreting cells (ASC) in intestinal mucosa and peripheral blo od was determined by the enzyme-linked immunospot (ELISPOT) assay befo re and after peroral vaccination with a B subunit-whole cell cholera v accine. Two groups of IgAd individuals, frequently infected and noninf ected respectively, and normal controls were studied. Before cholera v accination there were significantly higher frequencies of total IgM an d IgG ISC in the gut, but not in the blood, in the IgAd individuals th an in the controls. However, there were no significant differences bet ween healthy and infection-prone IgAd individuals in this respect. In response to oral cholera vaccination, intestinal cholera toxin (CT)-sp ecific IgG and IgM ASC were significantly more abundant among the IgAd individuals with a history of frequent infections than among the heal thy IgAd individuals and controls. A similar difference in IgG and IgM ASC, although not significant, was also noted in blood. In IgAd indiv iduals with frequent infections the vaccine induced variable anti-CT I gM ASC responses in the gut, ranging from no increase to a few strikin gly high responses. In the controls, the CT-specific responses were do minated by IgA ASC. The data show that oral cholera vaccination evoked strong CT-specific IgG ASC responses, and in some cases also strong I gM ASC responses in the intestinal mucosa of IgAd patients with a hist ory of frequent infections. The healthy IgAd individuals unexpectedly responded with lower numbers of CT-specific IgG ASC and did not show a ny increase of CT-specific IgM ASC in the intestinal mucosa. Thus, ina bility to mount a mucosal immune response to an oral antigen cannot in itself explain recurrent infections among many IgAd individuals.