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Author Notes:

Correspondence: Aftab A. Ansari, Room, 2309 WMB, Emory University School of Medicine, 101, Woodruff Circle, Atlanta, GA 30322; Email: pathaaa@emory.edu

Acknowledgments: The authors are grateful for the excellent support from the veterinary staff of the Yerkes National Primate Research Center of Emory University and

Subject:

Research Funding:

Supported by NIH RO1 AI 27057 and by the Thailand Research Fund

The authors are grateful to the Division of Research Resources of the NIH for their support of the Primate Center by the base grant RR-00165.

Keywords:

  • Siglec
  • non-human primate
  • SIV infection
  • monocytes
  • hematopoietic cell lineages

Differences in the Constitutive and SIV Infection Induced Expression of Siglecs by Hematopoietic Cells from Non-Human Primates

Tools:

Journal Title:

Cellular Immunology

Volume:

Volume 250, Number 1-2

Publisher:

, Pages 91-104

Type of Work:

Article | Post-print: After Peer Review

Abstract:

The expression of the Siglec family of molecules by hematopoietic cells from uninfected and SIV infected disease susceptible rhesus macaques (RM) and SIV infected disease resistant sooty mangabeys (SM) and for comparison humans was carried out. The predominant cell lineage in all 3 species expressing Siglec’s was monocytes. The major finding by both a cross sectional and a prospective SIV infection study showed that whereas monocytes from RM show marked increase in each Siglec constitutively expressed, monocytes from SM showed marked decreases in Siglec-1 expression. While monocytes from all 3 species constitutively expressed Siglec-3, human monocytes in addition expressed Siglec-5 and 9 and to a lower density 7, monocytes from RM expressed Siglec-7 and those from SM expressed Siglec-1. Monocytes from all 3 species however expressed mRNA for Siglec’s-1, 5, 7 and 9. The reasons for the failure to detect these molecules at the protein level and the mechanisms for such distinct effects of SIV infection on Siglec expression are discussed.

Copyright information:

© 2008 Elsevier Inc. All rights reserved.

This is an Open Access work distributed under the terms of the Creative Commons Attribution-NonCommerical-NoDerivs 3.0 Unported License (http://creativecommons.org/licenses/by-nc-nd/3.0/).

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