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alphabeta versus gammadelta fate choice: counting the T-cell lineages at the branch point Kreslavsky T; Gleimer M; Garbe AI; von Boehmer HImmunol Rev 2010[Nov]; 238 (1): 169-81Both alphabeta and gammadelta T cells develop in the thymus from a common progenitor. Historically distinguished by their T-cell receptor (TCR), these lineages are now defined on the basis of distinct molecular programs. Intriguingly, in many transgenic and knockout systems these programs are mismatched with the TCR type, leading to the development of gammadelta lineage cells driven by alphabetaTCR and vice versa. These puzzling observations were recently explained by the demonstration that TCR signal strength, rather than TCR type per se, instructs lineage fate, with stronger TCR signal favoring gammadelta and weaker signal favoring alphabeta lineage fates. These studies also highlighted the ERK (extracellular signal regulated kinase)-Egr (early growth response)-Id3 (inhibitor of differentiation 3) axis as a potential molecular switch downstream of TCR that determines lineage choice. Indeed, removal of Id3 was sufficient to redirect TCRgammadelta transgenic cells to the alphabeta lineage, even in the presence of strong TCR signal. However, in TCR non-transgenic Id3 knockout mice the overall number of gammadelta lineage cells was increased due to an outgrowth of a Vgamma1Vdelta6.3 subset, suggesting that not all gammadelta T cells depend on this molecular switch for lineage commitment. Thus, the gammadelta lineage may in fact be a collection of two or more lineages not sharing a common molecular program and thus equipollent to the alphabeta lineage. TCR signaling is not the only factor that is required for development of alphabeta and gammadelta lineage cells; other pathways, such as signaling from Notch and CXCR4 receptors, cooperate with the TCR in this process.|Animals[MESH]|Cell Differentiation/genetics[MESH]|Cell Lineage/genetics[MESH]|Humans[MESH]|Inhibitor of Differentiation Proteins/genetics/immunology[MESH]|Mice[MESH]|Mice, Knockout[MESH]|Mice, Transgenic[MESH]|Protein Binding/immunology[MESH]|Receptor Cross-Talk/immunology[MESH]|Receptors, Antigen, T-Cell, alpha-beta/*immunology[MESH]|Receptors, Antigen, T-Cell, gamma-delta/*immunology[MESH]|Signal Transduction/immunology[MESH]|T-Lymphocytes/*immunology[MESH] |
