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Rita Carsetti, Annalisa Pantosti, Isabella Quinti, Impairment of the Antipolysaccharide Response in Splenectomized Patients Is Due to the Lack of Immunoglobulin M Memory B Cells, The Journal of Infectious Diseases, Volume 193, Issue 8, 15 April 2006, Pages 1189–1190, https://doi.org/10.1086/501375
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To the Editor—In the abstract of their article entitled “Administration of protein-conjugate pneumococcal vaccine to patients who have invasive disease after splenectomy despite their having received 23-valent pneumococcal polysaccharide vaccine” [1], Musher et al. describe “2 patients who had recurring pneumococcal bacteremia after undergoing splenectomy despite having received numerous doses of PPV-23” (p. 1063). In the Discussion, they say that “Neither patient had IgG to [polysaccharides], and each had at least 1 bout of overwhelming pneumococcal sepsis caused by a vaccine serotype” (p. 1066). Interestingly, natural infection also failed to stimulate production of IgG. Heptavalent protein-conjugate pneumococcal vaccine (PCPV-7) was then administered, and it induced high levels of IgG to all 7 polysaccharides. Their finding raises interesting questions about the biological nature of the immune response to polysaccharide antigen
Recently, we studied the biological mechanisms responsible for the increased susceptibility to encapsulated bacterial infections in several clinical conditions. Although our understanding of human B cell development and B cell subsets is still limited, some relevant pieces of the puzzle are already in our hands. Here, we summarize our findings on human B cell defense against pneumococcal infection