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Molecular and Cellular Biology, February 2006, p. 1549-1557, Vol. 26, No. 4
0270-7306/06/$08.00+0     doi:10.1128/MCB.26.4.1549-1557.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Sialoadhesin-Deficient Mice Exhibit Subtle Changes in B- and T-Cell Populations and Reduced Immunoglobulin M Levels

Cornelia Oetke,1 Mary C. Vinson,2 Claire Jones,1 and Paul R. Crocker1*

The Wellcome Trust Biocentre, School of Life Sciences, University of Dundee, Dundee, United Kingdom,1 Neurology Centre of Excellence for Drug Discovery, GlaxoSmithKline, Essex, United Kingdom2

Received 25 August 2005/ Returned for modification 23 October 2005/ Accepted 30 November 2005

Sialoadhesin (Sn, also called Siglec-1 or CD169) is a transmembrane receptor and the prototypic member of the Siglec family of sialic acid binding immunoglobulin-like lectins. It is expressed on specialized subsets of resident macrophages in hematopoietic and lymphoid tissues and on inflammatory macrophages. In order to investigate its function, we generated Sn-deficient mice and confirmed that these mice are true nulls by fluorescence-activated cell sorter analysis and immunohistochemistry. Mice deficient in Sn were viable and fertile and showed no developmental abnormalities. Analysis of cell populations revealed no differences in bone marrow, peritoneal cavity, and thymus, but there was a small increase in CD8 T cells and a decrease in B220-positive cells in spleens and lymph nodes of Sn-deficient mice. Furthermore, in spleen there was a slight decrease in follicular B cells with an increase in numbers of marginal zone B cells. B- and T-cell maturation as well as responses to stimulation with thioglycolate were only slightly affected by Sn deficiency. Immunoglobulin titers in Sn-deficient mice were significantly decreased for immunoglobulin M (IgM) but similar for IgG subclasses. These results suggest a role for sialoadhesin in regulating cells of the immune system rather than in influencing steady-state hematopoiesis.

* Corresponding author. Mailing address: The Wellcome Trust Biocentre, University of Dundee, Dow Street, Dundee DD1 5EH, United Kingdom. Phone: 44-1382-345781. Fax: 44-1382-345783. E-mail: p.r.crocker{at}dundee.ac.uk.

Molecular and Cellular Biology, February 2006, p. 1549-1557, Vol. 26, No. 4
0022-538X/06/$08.00+0     doi:10.1128/MCB.26.4.1549-1557.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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