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Immunity
Article
License: Elsevier Non-Commercial
Data sources: UnpayWall
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Immunity
Article . 1996
License: Elsevier Non-Commercial
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Immunity
Article . 1996 . Peer-reviewed
License: Elsevier Non-Commercial
Data sources: Crossref
Immunity
Article . 1997
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αβ T Cell Development Is Abolished in Mice Lacking Both Lck and Fyn Protein Tyrosine Kinases

Authors: Deborah Finlay; Bente Lowin-Kropf; Arthur Weiss; Kari Connolly; Nicolai S. C. van Oers;

αβ T Cell Development Is Abolished in Mice Lacking Both Lck and Fyn Protein Tyrosine Kinases

Abstract

Two families of protein tyrosine kinases (PTKs), the Src and Syk/ZAP-70 families, are required for T cell development. Lck is the major Src family member required for thymopoiesis, since there is a severe deficit of CD4+CD8+ thymocytes and mature T cells in its absence. However, some peripheral T cells are evident in these mice, suggesting that additional PTKs may contribute to T cell development. Here we show that the combined disruption of Lck and Fyn (lck(-/-)fyn(-/-)) completely arrests alpha beta T cell development at the CD4-CD8- stage. The development of V gamma 3+ dendritic epidermal T cells is also severely impaired, but natural killer cell development and cytolytic activity is unaffected in lck(-/-)fyn(-/-) mice. These findings reveal the potential for redundant functions mediated by Src family PTKs while emphasizing crucial roles for Lck and Fyn in T cell development.

Keywords

Receptors, Antigen, T-Cell, alpha-beta, Immunology, Cell Differentiation, Protein-Tyrosine Kinases, Lymphocyte Activation, Proto-Oncogene Proteins c-fyn, Mice, Mutant Strains, Mice, Inbred C57BL, Mice, Infectious Diseases, src-Family Kinases, Lymphocyte Specific Protein Tyrosine Kinase p56(lck), T-Lymphocyte Subsets, Proto-Oncogene Proteins, Immunology and Allergy, Animals

  • BIP!
    Impact byBIP!
    citations
    This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    285
    popularity
    This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
    Top 10%
    influence
    This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    Top 1%
    impulse
    This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
    Top 1%
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citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
285
Top 10%
Top 1%
Top 1%
hybrid