Cutting edge: NKT cell development is selectively impaired in Fyn- deficient mice
| Autor: | Gerard Eberl, Lowin-Kropf B, Hr, Macdonald |
|---|---|
| Přispěvatelé: | Hugot, Bérengère, Ludwig Institute for Cancer Research |
| Jazyk: | angličtina |
| Rok vydání: | 1999 |
| Předmět: |
[SDV.IMM] Life Sciences [q-bio]/Immunology
Receptors Antigen T-Cell alpha-beta Immunology Receptors Antigen T-Cell Mice Transgenic chemical and pharmacologic phenomena Lymphocyte Activation Proto-Oncogene Proteins c-fyn Mice T-Lymphocyte Subsets Proto-Oncogene Proteins Immunology and Allergy Animals Antigens Ly Lectins C-Type Lymphocyte Count Antigens Mice Knockout Proteins Cell Differentiation hemic and immune systems Killer Cells Natural Mice Inbred C57BL Organ Specificity Antigens Surface CD4 Antigens NK Cell Lectin-Like Receptor Subfamily B Signal Transduction |
| Zdroj: | Journal of Immunology Journal of Immunology, American Association of Immunologists, 1999, pp.4091-4 Europe PubMed Central |
| ISSN: | 0022-1767 1550-6606 |
| Popis: | Most NK1.1+ T (NKT) cells express a biased TCRαβ repertoire that is positively selected by the monomorphic MHC class I-like molecule CD1d. The development of CD1d-dependent NKT cells is thymus dependent but, in contrast to conventional T cells, requires positive selection by cells of hemopoietic origin. Here, we show that the Src protein tyrosine kinase Fyn is required for development of CD1d-dependent NKT cells but not for the development of conventional T cells. In contrast, another Src kinase, Lck, is required for the development of both NKT and T cells. Impaired NKT cell development in Fyn-deficient mice cannot be rescued by transgenic expression of CD8, which is believed to increase the avidity of CD1d recognition by NKT cells. Taken together, our data reveal a selective and nonredundant role for Fyn in NKT cell development. |
| Databáze: | OpenAIRE |
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