Limited Ability of Antigen-Specific Th1 Responses to Inhibit Th2 Cell Development In Vivo

Th1 and Th2 cells mutually antagonize each other's differentiation. Consequently, allergen-specific Th1 cells are believed to be able to suppress the development of Th2 cells and to prevent the development of atopic disorders. To determine whether a pre-existing Ag-specific Th1 response can aff...

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Veröffentlicht in:The Journal of immunology (1950) 2005-02, Vol.174 (3), p.1325-1331
Hauptverfasser: Yasumi, Takahiro, Katamura, Kenji, Okafuji, Ikuo, Yoshioka, Takakazu, Meguro, Taka-aki, Nishikomori, Ryuta, Kusunoki, Takashi, Heike, Toshio, Nakahata, Tatsutoshi
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container_end_page 1331
container_issue 3
container_start_page 1325
container_title The Journal of immunology (1950)
container_volume 174
creator Yasumi, Takahiro
Katamura, Kenji
Okafuji, Ikuo
Yoshioka, Takakazu
Meguro, Taka-aki
Nishikomori, Ryuta
Kusunoki, Takashi
Heike, Toshio
Nakahata, Tatsutoshi
description Th1 and Th2 cells mutually antagonize each other's differentiation. Consequently, allergen-specific Th1 cells are believed to be able to suppress the development of Th2 cells and to prevent the development of atopic disorders. To determine whether a pre-existing Ag-specific Th1 response can affect the development of Th2 cells in vivo, we used an immunization model of Ag-pulsed murine dendritic cell (DC) transfer to induce distinct Th responses. When transferred into naive mice, Ag-pulsed CD8alpha(+) DCs induced a Th1 response and the production of IgG2a, whereas CD8alpha(-) DCs primed a Th2 response and the production of IgE. In the presence of a pre-existing Ag-specific Th2 environment due to Ag-pulsed CD8alpha(-) DC transfer, CD8alpha(+) DCs failed to prime Th1 cells. In contrast, CD8alpha(-) DCs could prime a Th2 response in the presence of a pre-existing Ag-specific Th1 environment. Moreover, exogenous IL-4 abolished the Th1-inducing potential of CD8alpha(+) DCs in vitro, but the addition of IFN-gamma did not effectively inhibit the potential of CD8alpha(-) DCs to prime IL-4-producing cells. Thus, Th1 and Th2 cells differ in their potential to inhibit the development of the other. This suggests that the early induction of allergen-specific Th1 cells before allergy sensitization will not prevent the development of atopic disorders.
doi_str_mv 10.4049/jimmunol.174.3.1325
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Consequently, allergen-specific Th1 cells are believed to be able to suppress the development of Th2 cells and to prevent the development of atopic disorders. To determine whether a pre-existing Ag-specific Th1 response can affect the development of Th2 cells in vivo, we used an immunization model of Ag-pulsed murine dendritic cell (DC) transfer to induce distinct Th responses. When transferred into naive mice, Ag-pulsed CD8alpha(+) DCs induced a Th1 response and the production of IgG2a, whereas CD8alpha(-) DCs primed a Th2 response and the production of IgE. In the presence of a pre-existing Ag-specific Th2 environment due to Ag-pulsed CD8alpha(-) DC transfer, CD8alpha(+) DCs failed to prime Th1 cells. In contrast, CD8alpha(-) DCs could prime a Th2 response in the presence of a pre-existing Ag-specific Th1 environment. 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subjects Adoptive Transfer
Animals
CD8 Antigens - biosynthesis
Cell Communication - immunology
Cell Differentiation - immunology
Dendritic Cells - immunology
Dendritic Cells - metabolism
Dendritic Cells - transplantation
Epitopes, T-Lymphocyte - immunology
Growth Inhibitors - pharmacology
Growth Inhibitors - physiology
Immunoglobulin G - biosynthesis
Immunosuppression
Interferon-gamma - biosynthesis
Interferon-gamma - physiology
Interleukin-4 - biosynthesis
Interleukin-4 - pharmacology
Mice
Mice, Inbred BALB C
Mice, Transgenic
Resting Phase, Cell Cycle - immunology
Spleen - cytology
Spleen - immunology
Spleen - metabolism
T-Lymphocytes, Helper-Inducer - cytology
T-Lymphocytes, Helper-Inducer - immunology
T-Lymphocytes, Helper-Inducer - metabolism
Th1 Cells - cytology
Th1 Cells - immunology
Th1 Cells - metabolism
Th2 Cells - cytology
Th2 Cells - immunology
Th2 Cells - metabolism
title Limited Ability of Antigen-Specific Th1 Responses to Inhibit Th2 Cell Development In Vivo
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