A two-step model of T cell subset commitment: antigen-independent commitment of T cells before encountering nominal antigen during pathogenic infections
| Autor: | Fengzhi Liu, Makoto Kanoh, Kohsuke Sumita, Yoshihiro Asano, Saho Maruyama, Teruyoshi Uetani, Hirokazu Sakan |
|---|---|
| Rok vydání: | 2002 |
| Předmět: |
Ovalbumin
T cell Immunology Antigen-Presenting Cells Gene Expression Mice Transgenic GATA3 Transcription Factor Biology Interleukin 21 Interferon-gamma Mice T-Lymphocyte Subsets medicine Immunology and Allergy Cytotoxic T cell Animals Listeriosis IL-2 receptor Antigens Antigen-presenting cell Mice Knockout Mice Inbred BALB C ZAP70 Models Immunological CD28 Cell Differentiation General Medicine Natural killer T cell Interleukin-12 Cell biology DNA-Binding Proteins Killer Cells Natural medicine.anatomical_structure Trans-Activators Receptors Chemokine Interleukin-4 Chemokines T-Box Domain Proteins Transcription Factors |
| Zdroj: | International immunology. 14(6) |
| ISSN: | 0953-8178 |
| Popis: | Pathogenic infections lead to activation of innate immunity followed by induction of a type 1 T cell subset and, therefore, provide a good model to evaluate when T cells commit to type 1 T cells. Here we show a two-step mechanism of T cell subset commitment during pathogenic infection. The first step is mediated by the basal function of macrophage/dendritic cells and is antigen independent. This step modulates the committed precursor frequency of T cell subsets and influences the expression of T-box expressed in T cells (T-bet) and GATA-3 genes. IL-12 and NK cells are not required for this step. The second step requires antigenic stimulation of T cells together with IL-12 or IL-4, and influences on the expression of T-bet and GATA-3. We propose a two-step T cell subset commitment pathway based on these observations. Therefore, pathogenic infections influence functional T cell commitment before T cells encounter nominal antigen. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|