Rita Carsetti, Licia Selleri and T. Neil Dear are Co-senior authors.
Development and function of the mammalian spleen†
Article first published online: 16 JAN 2007
Copyright © 2007 Wiley Periodicals, Inc.
Volume 29, Issue 2, pages 166–177, February 2007
How to Cite
Brendolan, A., Rosado, M. M., Carsetti, R., Selleri, L. and Dear, T. N. (2007), Development and function of the mammalian spleen. Bioessays, 29: 166–177. doi: 10.1002/bies.20528
- Issue published online: 16 JAN 2007
- Article first published online: 16 JAN 2007
- Work related to this review was supported by grants from the National Institutes of Health (HD43997) and from the March of Dimes and Birth Defects Foundation (6-FY03-071) to L.S. L.S. is an Irma T. Hirschl Scholar and the grateful recipient of an Alice Bohmfalk Charitable Trust research grant
The vertebrate spleen has important functions in immunity and haematopoiesis, many of which have been well studied. In contrast, we know much less about the mechanisms governing its early embryonic development. However, as a result of work over the past decade-mostly using knockout mice–-significant progress has been made in unravelling the genetic processes governing the spleen's early development. Key genetic regulators, such as Tlx1 and Pbx1, have been identified, and we know some of the early transcriptional hierarchies that control the early patterning and proliferation of the splenic primordium. In mouse and humans, asplenia can arise as a result of laterality defects, or the spleen can be absent with no other discernible abnormalities. Surprisingly, given the spleen's diverse functions, asplenic individuals suffer no major haematopoietic or immune defects apart from a susceptibility to infection with encapsulated bacteria. Recent evidence has shed light on a previously unknown role of the spleen in the development and maintenance of specific B cell populations that are involved in the initial response to infection caused by encapsulated bacteria. The lack of these populations in asplenic mice and humans may go some way to explaining this susceptibility. BioEssays 29: 166–177, 2007. © 2007 Wiley Periodicals, Inc.