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Induction of latency‐associated peptide (transforming growth factor‐β 1 ) expression on CD4 + T cells reduces Toll‐like receptor 4 ligand‐induced tumour necrosis factor‐α production in a transforming growth factor‐β‐dependent manner
Author(s) -
Boswell Sandra,
Sharif Shayan,
Alisa Akeel,
Pereira Stephen P.,
Williams Roger,
Behboudi Shahriar
Publication year - 2011
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2011.03425.x
Subject(s) - transforming growth factor , latency (audio) , receptor , toll like receptor , tumor necrosis factor alpha , biology , microbiology and biotechnology , peptide , cancer research , ligand (biochemistry) , chemistry , immunology , genetics , biochemistry , computer science , telecommunications , innate immune system
Summary CD4 + T cells expressing the latent form of transforming growth factor‐β [latency‐associated peptide (LAP) (TGF‐β 1 )] play an important role in the modulation of immune responses. Here, we identified a novel peptide ligand (GPC 81–95 ) with an intrinsic ability to induce membrane‐bound LAP (TGF‐β 1 ) expression on a subpopulation of human CD4 + T cells (using flow cytometry; ranging from 0·8% to 2·6%) and stimulate peripheral blood mononuclear cells to release LAP (TGF‐β 1 ) (using ELISPOT assay; ranging from 0·03% to 0·16%). In spite of this low percentage of responding cells, GPC 81–95 significantly reduced Toll‐like receptor 4 ligand‐induced tumour necrosis factor‐α production in a TGF‐β 1 ‐ and CD4 + T‐cell‐dependent manner. The results demonstrate that GPC 81–95 is a useful tool to study the functional properties of a subpopulation of LAP (TGF‐β 1 ) + CD4 + T cells and suggest a pathway that can be exploited to suppress inflammatory response.