Authors: Harn, Donald A.; McDonald, Jasmine; Atochina, Olga; Da'dara, Akram A.

Source: Immunological Reviews, Volume 230, Number 1, July 2009 , pp. 247-257(11)

Publisher: Wiley-Blackwell

Abstract:

Summary: 

Parasitic infections regulate/alter host immune responses. Among parasitic infections, helminth infection often leads to systemic immune suppression or anergy. Helminth infection or helminth extracts drive CD4⁺ T-helper (Th) cell responses towards Th2 type and activate antigen-presenting cells (APCs) such that these cells express an anti-inflammatory phenotype. Among the myriad molecules present on or secreted by helminth parasites, glycans have been shown to be key in inducing Th2-type and anti-inflammatory immune responses. The majority of studies on immune modulatory helminth glycans have focused on Lacto-N-fucopentaose III and Lewis^X. When presented as glycol-conjugates, with multiple copies of the sugars conjugated to a carrier molecule, these compounds activate APCs, inducing an alternative activation pattern, whose phenotypic profile is substantially different than that seen using pro-inflammatory activators such as lipopolysaccharide. Though the mechanism of APC activation by LNFPIII/Lewis^X glycoconjugates has not been fully elucidated, it involves C-type lectin ligation on the surface of APCs, with subsequent antagonism of Toll-like receptor signaling. In this article, we discuss the APC surface receptors known to play roles in LNFPIII/Lewis^X induced alternative activation of APCs. We also discuss what is currently known regarding downstream signaling pathways, closing with a discussion of future research directions for this field of investigation including the potential use of immune modulatory glycans as vaccine adjuvants and anti-inflammatory therapeutics.

Keywords: B-1 cells; dendritic cells; alternatively activated macrophages; T-helper cells; Toll-like receptor; Lacto-N-fucopentaose III

Document Type: Research article

DOI: http://dx.doi.org/10.1111/j.1600-065X.2009.00799.x

Affiliations: 1: Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA, USA.

Publication date: 2009-07-01

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