Format

Send to

Choose Destination
Glycobiology. 2014 Sep;24(9):818-25. doi: 10.1093/glycob/cwu067. Epub 2014 Jul 4.

The interplay between Siglecs and sialylated pathogens.

Author information

1
Glycobiology Research and Training Center Department of Pediatrics.
2
Glycobiology Research and Training Center Department of Pediatrics Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, La Jolla, CA 92093, USA vnizet@ucsd.edu.

Abstract

Siglecs are mammalian sialic acid (Sia) recognizing immunoglobulin-like receptors expressed across the major leukocyte lineages, and function to recognize ubiquitous Sia epitopes on cell surface glycoconjugates and regulate immunological and inflammatory activities of these cells. A large subset referred to as CD33-related Siglecs are inhibitory receptors that limit leukocyte activation, and recent research has shown that the pathogen group B Streptococcus (GBS) binds to these Siglecs in Sia- and protein-dependent fashion to downregulate leukocyte bactericidal capacity. Conversely, sialoadhesin is a macrophage phagocytic receptor that engages GBS and other sialylated pathogens to promote effective phagocytosis and antigen presentation for the adaptive immune response. A variety of other important Siglec interactions with bacterial, viral and protozoan pathogens are beginning to be recognized. Siglec genes and binding specificities are rapidly evolving among primates, with key extant polymorphisms in human populations that may influence susceptibility to infection-associated disorders including chronic obstructive pulmonary disease and premature birth. This review summarizes current understanding of interactions between pathogens and Siglecs, a field of investigation that is likely to continue expanding in scope and medical importance.

KEYWORDS:

Siglec; bacterial pathogenesis; innate immunity; molecular mimicry, sialic acid

PMID:
24996821
PMCID:
PMC4168292
DOI:
10.1093/glycob/cwu067
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Silverchair Information Systems Icon for PubMed Central
Loading ...
Support Center