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LETTERS TO THE EDITOR |
Australian Research Council Special Research Centre for Functional and Applied Genomics, Institute for Molecular Bioscience, University of Queensland, Brisbane, Australia
The recent paper by Jang et al. (1), highlighted in In This Issue (2), is part of a recent rediscovery of the myeloid compartment of the intestinal lamina propria, which is probably the largest macrophage population in the body. The authors refer to these cells as dendritic cells, based on their expression of surface markers such as CD11c, but a dendritic cell was originally defined as a cell that can present Ag to naive T cells. The large majority of the stellate (or dendritic) cells of the intestinal lamina propria expresses the macrophage-specific F4/80 Ag, which is lost from mature Ag-representing cells, and also expresses the CSF-1 receptor and a CSF-1R-EGFP reporter gene (3) (see images of F4/80 and CSF-1R online
www.macrophages.com
). The majority of the so-called dendritic cells of the lamina propria is clearly phagocytic (1). Some 15 years ago, the myeloid cells of mouse lamina propria were isolated, and the cells that could actually stimulate naive T cells in a MLR were selectively enriched in the nonphagocytic population (4). By contrast, the F4/80-positive phagocytes, which were also strongly class II-MHC-positive, caused indomethacin-sensitive repression of T cell activation. It is inescapable that the large majority of the cells studied by Jang et al. (1) are not dendritic cells by the functional definition, and there is no evidence that all, or indeed any, of them ever become cells that can present Ag to naive T cells. They are the lamina propria macrophages. They might acquire Ag-presenting activity. On the other hand, they might actually be more important to the maintenance of tolerance.
References
This article has been cited by other articles:
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M. H. Jang and M. Miyasaka Response to Comment on "CCR7 Is Critically Important for Migration of Dendritic Cells in Intestinal Lamina Propria to Mesenteric Lymph Nodes" J. Immunol., August 15, 2006; 177(4): 2035 - 2036. [Full Text] [PDF] |
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