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Ly49-dependent NK cell licensing and effector inhibition involve the same interaction site on MHC ligands.

Publication ,  Journal Article
Choi, T; Ferris, ST; Matsumoto, N; Poursine-Laurent, J; Yokoyama, WM
Published in: J Immunol
April 1, 2011

NK cells become functionally competent to be triggered by their activation receptors through the interaction of NK cell inhibitory receptors with their cognate self-MHC ligands, an MHC-dependent educational process termed "licensing." For example, Ly49A(+) NK cells become licensed by the interaction of the Ly49A inhibitory receptor with its MHC class I ligand, H2D(d), whereas Ly49C(+) NK cells are licensed by H2K(b). Structural studies indicate that the Ly49A inhibitory receptor may interact with two sites, termed site 1 and site 2, on its H2D(d) ligand. Site 2 encompasses the α1/α2/α3 domains of the H2D(d) H chain and β(2)-microglobulin (β2m) and is the functional binding site for Ly49A in effector inhibition. Ly49C functionally interacts with a similar site in H2K(b). However, it is currently unknown whether this same site is involved in Ly49A- or Ly49C-dependent licensing. In this study, we produced transgenic C57BL/6 mice expressing wild-type or site 2 mutant H2D(d) molecules and studied whether Ly49A(+) NK cells are licensed. We also investigated Ly49A- and Ly49C-dependent NK licensing in murine β2m-deficient mice that are transgenic for human β2m, which has species-specific amino acid substitutions in β2m. Our data from these transgenic mice indicate that site 2 on self-MHC is critical for Ly49A- and Ly49C-dependent NK cell licensing. Thus, NK cell licensing through Ly49 involves specific interactions with its MHC ligand that are similar to those involved in effector inhibition.

Duke Scholars

Published In

J Immunol

DOI

EISSN

1550-6606

Publication Date

April 1, 2011

Volume

186

Issue

7

Start / End Page

3911 / 3917

Location

United States

Related Subject Headings

  • beta 2-Microglobulin
  • NK Cell Lectin-Like Receptor Subfamily C
  • NK Cell Lectin-Like Receptor Subfamily A
  • Models, Animal
  • Mice, Transgenic
  • Mice, Knockout
  • Mice, Inbred C57BL
  • Mice
  • Ligands
  • Killer Cells, Natural
 

Citation

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ICMJE
MLA
NLM
Choi, T., Ferris, S. T., Matsumoto, N., Poursine-Laurent, J., & Yokoyama, W. M. (2011). Ly49-dependent NK cell licensing and effector inhibition involve the same interaction site on MHC ligands. J Immunol, 186(7), 3911–3917. https://doi.org/10.4049/jimmunol.1004168
Choi, Taewoong, Stephen T. Ferris, Naoki Matsumoto, Jennifer Poursine-Laurent, and Wayne M. Yokoyama. “Ly49-dependent NK cell licensing and effector inhibition involve the same interaction site on MHC ligands.J Immunol 186, no. 7 (April 1, 2011): 3911–17. https://doi.org/10.4049/jimmunol.1004168.
Choi T, Ferris ST, Matsumoto N, Poursine-Laurent J, Yokoyama WM. Ly49-dependent NK cell licensing and effector inhibition involve the same interaction site on MHC ligands. J Immunol. 2011 Apr 1;186(7):3911–7.
Choi, Taewoong, et al. “Ly49-dependent NK cell licensing and effector inhibition involve the same interaction site on MHC ligands.J Immunol, vol. 186, no. 7, Apr. 2011, pp. 3911–17. Pubmed, doi:10.4049/jimmunol.1004168.
Choi T, Ferris ST, Matsumoto N, Poursine-Laurent J, Yokoyama WM. Ly49-dependent NK cell licensing and effector inhibition involve the same interaction site on MHC ligands. J Immunol. 2011 Apr 1;186(7):3911–3917.

Published In

J Immunol

DOI

EISSN

1550-6606

Publication Date

April 1, 2011

Volume

186

Issue

7

Start / End Page

3911 / 3917

Location

United States

Related Subject Headings

  • beta 2-Microglobulin
  • NK Cell Lectin-Like Receptor Subfamily C
  • NK Cell Lectin-Like Receptor Subfamily A
  • Models, Animal
  • Mice, Transgenic
  • Mice, Knockout
  • Mice, Inbred C57BL
  • Mice
  • Ligands
  • Killer Cells, Natural