We have previously shown that the antibody response to a T cell-dependent protein antigen, tetanus toxoid is reduced in patients having surgery. Because most bacterial antigens are not protein but polysaccharide, we studied in vivo and in vitro antibody responses to a relatively T cell-independent polysaccharide antigen, 23 valent pneumococcal polysaccharide (Pneumovax) (PPS). Subjects were classified by skin testing with five standard antigens as reactive patients (R, positive response to any antigen, N = 5), anergic patients (A, no response, N = 7) or laboratory controls (C, reactive personnel, N = 8). Blood lymphocytes taken before and after immunization with 0.5 ml PPS were cultured in vitro. Quantities of total and anti-PPS IgG, IgM, and IgA in culture supernatants and serum were measured by radioimmunoassay. There was no difference in in vivo anti-PPS production in the three groups (p greater than 0.05 for all comparisons, Wilcoxon rank-sum test). Positive response rates (greater than twofold increase) for all classes of immunoglobulin were also similar in the three groups (X2(2) = 0.36, 0.36, and 0.81 for IgG, IgM, and IgA, p greater than 0.05). In in vitro studies, peak quantities of IgA anti-PPS produced by A were significantly less than C (0.64 X divided by 0.41 versus 2.03 X divided by 0.6, p less than 0.05, Wilcoxon rank-sum test). Synthesis of all other classes of Ig anti-PPS and simultaneous measurement of total Ig (nanograms per culture) produced in vitro were not significantly different among all groups (p greater than 0.05, Wilcoxon rank-sum test). In C, R, and A, peak in vitro isotype-specific anti-PPS production correlated with the magnitude of the in vivo serum response (Spearman rank correlation = 0.53, 0.60, and 0.59 for IgG, IgM, and IgA, p less than 0.05). We conclude that these data show normal in vivo antibody responses to a relatively T cell-independent bacterial polysaccharide antigen in surgical patients and a good correlation of in vivo- to in vitro-specific antibody responses. The data imply that a T cell defect is responsible for reduced humoral immunity to protein antigens. Because most bacterial antigens are not protein but polysaccharides, active immunization of patients with bacterial vaccines may produce effective immunity.
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