B-1a B cells that link the innate and adaptive immune responses are lacking in the absence of the spleen

Hedda Wardemann, Thomas Boehm, Neil Dear, Rita Carsetti

Research output: Contribution to journalArticlepeer-review

Abstract

Splenectomized individuals are prone to overwhelming infections with encapsulated bacteria and splenectomy of mice increases susceptibility to streptococcal infections, yet the exact mechanism by which the spleen protects against such infections is unknown. Using congenitally asplenic mice as a model, we show that the spleen is essential for the generation of B-1a cells, a B cell population that cooperates with the innate immune system to control early bacterial and viral growth. Splenectomy of wild-type mice further demonstrated that the spleen is also important for the survival of B-1a cells. Transfer experiments demonstrate that lack of these cells, as opposed to the absence of the spleen per se, is associated with an inability to mount a rapid immune response against streptococcal polysaccharides. Thus, absence of the spleen and the associated increased susceptibility to streptococcal infections is correlated with lack of B-1a B cells. These findings reveal a hitherto unknown role of the spleen in generating and maintaining the B-1a B cell pool.

Original languageEnglish
Pages (from-to)771-780
Number of pages10
JournalJournal of Experimental Medicine
Volume195
Issue number6
DOIs
Publication statusPublished - Mar 18 2002

Keywords

  • Asplenia
  • B-1a cells
  • Hox11
  • Natural antibodies
  • Streptococcus pneumoniae

ASJC Scopus subject areas

  • Immunology

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