Talk:Cardiovascular System - Spleen Development: Difference between revisions
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==2007== | |||
===Development and function of the mammalian spleen=== | |||
Bioessays. 2007 Feb;29(2):166-77. | |||
Brendolan A, Rosado MM, Carsetti R, Selleri L, Dear TN. | |||
Department of Cell and Developmental Biology, Cornell University, Weill Medical School, New York, NY, USA. | |||
Abstract | |||
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. | |||
Copyright 2007 Wiley Periodicals, Inc. | |||
PMID: 17226804 | |||
Revision as of 16:19, 21 February 2011
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Cite this page: Hill, M.A. (2024, April 20) Embryology Cardiovascular System - Spleen Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Cardiovascular_System_-_Spleen_Development |
2009
Congenital anomalies of the spleen from an embryological point of view
Med Sci Monit. 2009 Dec;15(12):RA269-76.
Varga I, Galfiova P, Adamkov M, Danisovic L, Polak S, Kubikova E, Galbavy S. Department of Histology and Embryology, Faculty of Medicine, Comenius University in Bratislava, Slovak Republic.
Abstract The spleen is the major accumulation of lymphoid tissue in the human body, an organ which prenatally produces and postnatally controls blood cells. Normally, a developed spleen lies in the upper left quadrant in parallel with the long axis of the 10th rib. It is a mesodermal derivate which first appears as a condensation of mesenchymal cells inside the dorsal mesogastrium at the end of the fourth embryonic week. Some congenital anomalies of the spleen are common, such as splenic lobulation and accessory spleen, while other conditions are rare, such as wandering spleen and polysplenia. Splenogonadal fusion is also a rare developmental anomaly, resulting from abnormal fusion of the splenic and gonadal primordia during prenatal development. The purpose of this article is to describe the normal development of the human spleen, supplemented with our own photomicrographs and a review of congenital anomalies of the spleen with their possible embryonic basis.
PMID: 19946246
http://www.medscimonit.com/fulltxt.php?ICID=878269
2007
Development and function of the mammalian spleen
Bioessays. 2007 Feb;29(2):166-77.
Brendolan A, Rosado MM, Carsetti R, Selleri L, Dear TN.
Department of Cell and Developmental Biology, Cornell University, Weill Medical School, New York, NY, USA. Abstract 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.
Copyright 2007 Wiley Periodicals, Inc. PMID: 17226804
