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Review
. 2001 Jan 15;193(2):F5-9.
doi: 10.1084/jem.193.2.f5.

Differentiation of T regulatory cells by immature dendritic cells

M G Roncarolo  1 , M K Levings, C Traversari
Affiliations
Review

Differentiation of T regulatory cells by immature dendritic cells

M G Roncarolo et al. J Exp Med. .
No abstract available

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Figures

Figure 1
Figure 1
Control of peripheral tolerance to self-antigens. In the steady state, iDCs take up proteins from cells undergoing normal cell turnover (1a). In the absence of inflammatory signals, DCs remain immature but may still enter regional lymph nodes (2a). Precursors of Tr cells (Trp) encounter self-antigen on iDCs and are primed to become regulatory rather than effector T cells (3a). This step may require that antigen is “handed off” to specialized DCs (in blue), which are dedicated to priming Tr cells. Primed Tr cells home to the tissue and have suppressive effects, mediated by inhibitory cytokines and cell surface molecules, that ensure that DCs remain in an immature state in the absence of inflammation (4a). During an infection, iDCs take up self-antigens in the context of maturation signals (1b). mDCs migrate to regional lymph nodes (2b) and prime naive CD4+ or CD8+ T cells to become effector T cells (3b). Here, DC1 cells (in green) may polarize CD4+ cells toward a Th1 phenotype, whereas DC2 cells (in yellow) would polarize toward a Th2 phenotype. T effector cells migrate to the site of inflammation, where they are regulated by Tr cells (4b). CD4+ or CD8+ Tr cells specific for self-antigens regulate immune responses by producing immunoregulatory cytokines such as IL-10 and TGF-β or by directly suppressing activated Th1 cells via a mechanism that requires cell–cell contact.
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