{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T19:54:37Z","timestamp":1792180477823,"version":"4.4.0"},"reference-count":20,"publisher":"Rockefeller University Press","issue":"7","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2003,4,7]]},"abstract":"<jats:p>Splenectomized and asplenic patients have a high incidence of infections by encapsulated bacteria and do not respond to polysaccharide vaccines. To understand whether the absence of the spleen is associated with a defined B cell defect, we analyzed B cell subsets in the peripheral blood. We found that a population of B cells known as immunoglobulin (Ig)M memory is lacking in patients without spleen. The absence of IgM memory B cells correlates with an impaired immune response to encapsulated bacteria not only in splenectomized patients, but also in individuals with an intact spleen. We show that the physiological and transient predisposition to pneumococcal infections of young children (0\u20132 yr) is associated with the lack of circulating IgM memory B cells and of serum antipolysaccharide IgM. We also demonstrate that IgM memory B cells are undetectable in a fraction of patients with common variable immunodeficiency, who have recurrent and invasive infections by encapsulated bacteria. IgM memory B cells, therefore, require the spleen for their generation and\/or survival and are responsible for the protection against encapsulated bacteria.<\/jats:p>","DOI":"10.1084\/jem.20022020","type":"journal-article","created":{"date-parts":[[2003,4,7]],"date-time":"2003-04-07T16:34:31Z","timestamp":1049733271000},"page":"939-945","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":539,"title":["Human Immunoglobulin M Memory B Cells Controlling\n                    <i>Streptococcus pneumoniae<\/i>\n                    Infections Are Generated in the Spleen"],"prefix":"10.1084","volume":"197","author":[{"given":"Stephanie","family":"Kruetzmann","sequence":"first","affiliation":[{"name":"1Max-Planck Institute for Immunology, Department of Developmental Immunology, D-79108 Freiburg, Germany"},{"name":"5Division of Rheumatology and Clinical Immunology, University Hospital, D-79106 Freiburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. 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