The Journal of Experimental Medicine
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Published 18 March 2002. doi:10.1084/jem.20011140
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© Rockefeller University Press, 0022-1007/2002/3/771/ $5.00
The Journal of Experimental Medicine, Volume 195, Number 6, March 18, 2002 771-780

Original Article

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 and Rita Carsetti

Department of Developmental Immunology, Max-Planck Institute for Immunobiology, Freiburg 79108, Germany

Address correspondence to Rita Carsetti, Research Center Ospedale Bambino Gesù, University of Tor Vergata, Via di Tor Vergata 135, Rome 00133, Italy. Phone: 39-06-725-96825; Fax: 39-06-725-96822; E-mail: Rita.Carsetti{at}uniroma2.it

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.

Key Words: B-1a cells • asplenia • natural antibodies • Streptococcus pneumoniae • Hox11


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