CCR6 is not necessary for functional effects of human CCL18 in a mouse model

Irina G Luzina,Sergei P Atamas

doi:10.1186/1755-1536-5-2

Abstract

CCL18, a chemokine with no known receptor, has been implicated in several fibrotic pulmonary diseases associated with T-lymphocyte infiltration. It has been hypothesized that CCL18 may act through CCR6. Gene delivery of human CCL18 to the lungs of wild-type mice induced pulmonary infiltration of T-lymphocytes, less than 5% of which expressed CCR6. In the lungs of CCR6-deficient mice, CCL18-driven infiltration of T-lymphocytes was attenuated but not fully abrogated. It was concluded that CCR6 is not necessary for CCL18-induced changes in mice in vivo and that CCR6 is not the main functional receptor for CCL18 in this model.

Highlights

CC chemokine ligand 18 (CCL18), a chemokine with no known receptor, has been implicated in several fibrotic pulmonary diseases associated with T-lymphocyte infiltration
Correspondence CC chemokine ligand 18 (CCL18, termed MIP-4, PARC, AMAC-1, DC-CK-1 and SCYA18) is a chemokine that has been implicated in several fibrotic pulmonary diseases associated with T-lymphocyte infiltration [1,2,3,4,5]
We hypothesized that if chemokine receptor 6 (CCR6) is a receptor for CCL18, the effects of human CCL18 in mice [3,4,5,9] may be mediated by mouse CCR6

Summary

Introduction

CCL18, a chemokine with no known receptor, has been implicated in several fibrotic pulmonary diseases associated with T-lymphocyte infiltration. This cytokine has no known receptor and is present in humans but not in mice [6,7,8,9], human CCL18 is fully functionally active in mice in vivo, causing chemotaxis of T-lymphocytes [3,4,5,9]. These observations suggest that CCL18 was lost in mice after evolutionary separation from human ancestors, the receptor for it has been preserved in both mice and humans.

Results

Conclusion