University at Buffalo - The State University of New York
Skip to Content
Enhanced antigen uptake by dendritic cells induced by the B pentamer of the type II heat-labile enterotoxin LT-IIa requires engagement of TLR2. - PubMed - NCBI
Format

Send to

Choose Destination
See comment in PubMed Commons below
Vaccine. 2010 May 7;28(21):3696-705. doi: 10.1016/j.vaccine.2010.03.016. Epub 2010 Mar 21.

Enhanced antigen uptake by dendritic cells induced by the B pentamer of the type II heat-labile enterotoxin LT-IIa requires engagement of TLR2.

Author information

1
The Department of Microbiology and Immunology, The University at Buffalo, NY 14214, USA.

Abstract

The potent mucosal adjuvant properties of the type II heat-labile enterotoxin LT-IIa of Escherichia coli are dependent upon binding of the B pentamer of the enterotoxin (LT-IIa-B(5)) to ganglioside receptors on immunocompetent cells. To evaluate the immunomodulatory activities of LT-IIa-B(5), in vitro experiments employing bone marrow-derived dendritic cells (BMDC) were performed. Uptake of OVA-FITC, a model antigen (Ag), was enhanced by treatment of BMDC with LT-IIa-B5, but not by treatment of cells with the B pentamer of cholera toxin (CTB). Expression of co-stimulatory molecules (CD40, CD80, CD86, and MHC-II) and cytokines (IL-12p40, TNF-alpha, and IFN-gamma) was increased in BMDC treated with LT-IIa-B(5). The capacity of LT-IIa-B(5) to enhance Ag uptake and to induce expression of co-stimulatory receptors and cytokines by BMDC was dependent upon expression of TLR2 by the cell. Increased Ag uptake induced by LT-IIa-B(5) was correlated with increased Ag-specific proliferation of CD4(+) T cells in an in vitro syngeneic DO11.10 CD4(+) T cell proliferation assay. These experiments confirm that LT-IIa-B(5) exhibits potent immunomodulatory properties which may be exploitable as a non-toxic mucosal adjuvant.

PMID:
20332049
PMCID:
PMC2862118
DOI:
10.1016/j.vaccine.2010.03.016
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Support Center