Stimulation of Human CD4+ T Lymphocytes via TLR3, TLR5 and TLR7/8 Up-Regulates Expression of Costimulatory and Modulates Proliferation
Rita Simone1, 2, Antonio Floriani1, 3, Daniele Saverino1, *
Identifiers and Pagination:Year: 2009
First Page: 1
Last Page: 8
Publisher ID: TOMICROJ-3-1
Article History:Received Date: 28/11/2008
Revision Received Date: 5/12/2008
Acceptance Date: 30/12/2008
Electronic publication date: 15/1/2009
Collection year: 2009
open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.
The cells of innate and adaptive immunity, although activated by different ligands, engage in cross talk to ensure a successful immune outcome. Toll-like receptors (TLRs) are key components of the innate immune system and have the ability to detect microbial infection and trigger host defence responses. Otherwise, human T lymphocytes are able to produce most TLRs. Thus, we analyze the capability of some TLR ligands to modulate the function of highly-purified CD4+ T cells. We found that agents acting via TLRs (poly I:C, a TLR3 ligand; flagellin, a TLR5 ligand; and R848, a TLR7/8 ligand) are able to regulate the expression of costimulatory molecules both on purified antigen presenting cells and on purified T lymphocytes. Moreover, the activation mediated by TLRs determines a kinetic expression of B7-family members such as through an inhibition of T lymphocytes delayed proliferation. These findings suggest a functional role of some invading microorganisms in regulating acquired immunity.