Degranulation plays an essential part in regulating cell surface expression of Fas ligand in T cells and natural killer cells

10.1038/4779 ◽  
1999 ◽  
Vol 5 (1) ◽  
pp. 90-96 ◽  
Author(s):  
G. Bossi ◽  
G.M. Griffiths
Keyword(s):  
T Cells ◽  
Natural Killer Cells ◽  
Cell Surface ◽  
Natural Killer ◽  
Fas Ligand ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
Killer Cells

scholarly journals Antibody cooperative adsorption onto AuNPs and its exploitation to force natural killer cells to kill HIV-infected T cells

Nano Today ◽  
2021 ◽  
Vol 36 ◽  
pp. 101056
Author(s):  
Antonio Astorga-Gamaza ◽  
Michele Vitali ◽  
Mireya L. Borrajo ◽  
Rosa Suárez-López ◽  
Carlos Jaime ◽  
...  
Keyword(s):  
T Cells ◽  
Natural Killer Cells ◽  
Natural Killer ◽  
Killer Cells ◽  
Cooperative Adsorption

Impact of β2 integrin deficiency on mouse natural killer cell development and function

Blood ◽  
2011 ◽  
Vol 117 (10) ◽  
pp. 2874-2882 ◽  
Author(s):  
Karine Crozat ◽  
Céline Eidenschenk ◽  
Baptiste N. Jaeger ◽  
Philippe Krebs ◽  
Sophie Guia ◽  
...  
Keyword(s):  
Cell Surface ◽  
Nk Cells ◽  
Natural Killer ◽  
Nk Cell ◽  
Surface Expression ◽  
Cell Maturation ◽  
Cell Surface Expression ◽  
Mcmv Infection ◽  
Β2 Integrin

Abstract Natural killer (NK) cells are innate immune cells that express members of the leukocyte β2 integrin family in humans and mice. These CD11/CD18 heterodimers play critical roles in leukocyte trafficking, immune synapse formation, and costimulation. The cell-surface expression of one of these integrins, CD11b/CD18, is also recognized as a major marker of mouse NK-cell maturation, but its function on NK cells has been largely ignored. Using N-ethyl-N-nitrosourea (ENU) mutagenesis, we generated a mouse carrying an A → T transverse mutation in the Itgb2 gene, resulting in a mutation that prevented the cell-surface expression of CD18 and its associated CD11a, CD11b, and CD11c proteins. We show that β2 integrin–deficient NK cells have a hyporesponsive phenotype in vitro, and present an alteration of their in vivo developmental program characterized by a selective accumulation of c-kit+ cells. NK-cell missing-self recognition was partially altered in vivo, whereas the early immune response to mouse cytomegalovirus (MCMV) infection occurred normally in CD18-deficient mice. Therefore, β2 integrins are required for optimal NK-cell maturation, but this deficiency is partial and can be bypassed during MCMV infection, highlighting the robustness of antiviral protective responses.

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