Antigen dose, type of antigen‐presenting cell and time of differentiation contribute to the T helper 1/T helper 2 polarization of naive T cells

Summary Antigenic encounter by T cells induces immunological synapse formation and T‐cell activation. Using different concentrations of toxic shock syndrome toxin‐1 (TSST‐1) as stimulus, we examined the capacities of dendritic cells (DC) and macrophages (Mφ) to prime syngeneic naive T cells. DCs wer...

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Bibliographic Details
Published inImmunology Vol. 110; no. 4; pp. 430 - 439
Main Authors Rothoeft, T., Gonschorek, A., Bartz, H., Anhenn, O., Schauer, U.
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Science Ltd 01.12.2003
Wiley Subscription Services, Inc
Blackwell Science Inc
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Summary:Summary Antigenic encounter by T cells induces immunological synapse formation and T‐cell activation. Using different concentrations of toxic shock syndrome toxin‐1 (TSST‐1) as stimulus, we examined the capacities of dendritic cells (DC) and macrophages (Mφ) to prime syngeneic naive T cells. DCs were, under all experimental settings, more efficient than Mφ at clustering T cells. Translocation of the T‐cell receptor (TCR) to the contact area was found to be induced by DCs, as well as by Mφ, in an antigen‐dependent manner, although Mφ were less efficient at inducing TCR translocation. Capping of protein kinase C θ (PKCθ) was also antigen dependent but induced exclusively by DCs. Likewise, DCs were found to be more potent inducers of interleukin‐2 (IL‐2) production and proliferation of naive T cells than Mφ. After 3 days of culture, DCs presenting 100 ng/ml TSST‐1 induced interferon‐γ (IFN‐γ)‐secreting cells, whereas Mφ did not. After 7 days of culture, DCs presenting 0·1 ng/ml TSST‐1, and Mφ presenting high (as well as low) doses of TSST‐1, induced IL‐4‐producing cells. We therefore provide evidence to show that antigen dose, type of antigen‐presenting cell and time of differentiation can contribute to T‐cell differentiation.
ISSN:0019-2805
1365-2567
DOI:10.1111/j.1365-2567.2003.01758.x