H3N2 Influenza Infection Elicits More Cross-Reactive and Less Clonally Expanded Anti-Hemagglutinin Antibodies Than Influenza Vaccination (original) (raw)
Figure 1
Characterization of peripheral blood plasmacytosis 7 days after TIV or EI.
A. Peripheral blood B cells (CD3/14/16/235a− CD19+) stained for plasma cell markers (CD3/14/16/235a− CD19+ CD20−/lo CD27hi CD38hi); points shown are percentage of B cells that were plasma cells. TIV mean 2.75%±0.90%; EI mean 2.26±0.74%; two-tailed t test, p = 0.68. B. Human rmAbs derived from sorted plasma cells tested for reactivity. From TIV subjects, 252/404 rmAbs (62.4%) reacted with ≥1 influenza antigen (blue wedge), 152/404 (37.6%) did not react with any tested rHA or split-virus antigen (gray wedge). From EI subjects, 37/451 rmAbs (8.2%) reacted with ≥1 influenza antigen (tested vs. TIV, χ2 = 279.5, p<0.0001), 414/451 (91.8%) did not react with any tested rHA or split-virus antigen. C. Human rmAbs membership in clonal lineages. From TIV subjects, 175/404 (43.3%) rmAbs were members of 46 clonal lineages (red wedge); from EI subjects, 28/451 (6.2%) rmAbs were members of 12 clonal lineages (χ2 = 162.1, p<0.0001).