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Volume 84, Issue 2, Pages 133-144 (March 2010)


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IgG is transported across the mouse yolk sac independently of FcγRIIb

Sudhasri Mohantya1, Jonghan Kimab12, Latha P. Ganesana, Gary S. Phillipsc, Keding Huac, David Jarjourac, William L. Haytonb, John M. Robinsond, Clark L. AndersonaCorresponding Author Informationemail addressweb address

Received 26 August 2009; received in revised form 28 October 2009; accepted 30 October 2009. published online 23 November 2009.

Abstract 

While generally accepted that FcRn of the human syncytiotrophoblast and the mouse yolk sac endoderm is the major IgG transporter, the finding of a different Fc receptor FcγRIIb (RIIb) in the human placental endothelium has suggested the existence of an additional IgG transporter. Testing our hypothesis in mouse, we found that while RIIb is expressed in the yolk sac vasculature, IgG concentrations in fetuses of wild-type mice (RIIb+/+) and mice with a null mutation in the gene encoding RIIb (RIIb−/− mice) are not different, and we thus reject our hypothesis that yolk sac RIIb transports IgG in utero in the mouse. However, the capillary bed in the mouse yolk sac is structurally more complex than in human placenta, consisting of three types of cells: an RIIb-negative endothelium, a unique RIIb-bearing cell that also expresses 2 out of 4 macrophage markers but not endothelial cell or pericyte markers, and pericytes. As in the human placenta the b2 isoform of RIIb predominates in the mouse yolk sac. Remarkably only a single capillary channel rather than 2 channels with a loop is found in each yolk sac villus, which, along with intracapillary erythrocytes, suggests that blood flow is peristaltic, mediated by pericytes. It is not clear whether RIIb in the human placental villus might mediate an IgG transport function in light of the mouse yolk sac equivalent failing to do so.

a Department of Internal Medicine, The Ohio State University, Columbus, OH 43210, USA

b College of Pharmacy, The Ohio State University, Columbus, OH 43210, USA

c Center for Biostatistics, The Ohio State University, Columbus, OH 43210, USA

d Department of Physiology and Cell Biology, The Ohio State University, Columbus, OH 43210, USA

Corresponding Author InformationCorresponding author at: Department of Internal Medicine, The Ohio State University, 012K Davis Heart and Lung Research Institute, 473 West Twelfth Avenue, Columbus, OH 43210, USA. Tel.: +1 614 247 7650; fax: +1 614 247 7669.

1 These authors contributed equally.

2 Present address: Harvard School of Public Health, Department of Genetics & Complex Diseases, 665 Huntington Avenue, Boston, MA 02115, USA.

PII: S0165-0378(09)00526-9

doi:10.1016/j.jri.2009.10.008


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