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Generation of Knock-out Primary and Expanded Human NK Cells Using Cas9 Ribonucleoproteins
Published on: June 14, 2018
A Y chromosome-linked factor impairs NK T development.
Johnna D Wesley1, Marlowe S Tessmer, Christophe Paget
1Department of Molecular Microbiology and Immunolog, Division of Biology and Medicine, Brown University, Providence, RI 02912, USA.
Journal of Immunology (Baltimore, Md. : 1950)
|September 6, 2007
Summary
The Y chromosome, not interferon signaling, is crucial for invariant Natural Killer T (iNKT) cell development in male mice. This finding reveals a novel genetic influence on these unique innate immune cells.
Area of Science:
- Immunology
- Innate Immunity
- T cell Biology
Background:
- Invariant Natural Killer T (iNKT) cell development differs from conventional T cell selection.
- The genetic factors governing iNKT cell ontogeny remain largely unknown.
Purpose of the Study:
- To investigate the genetic basis for the development of Valpha14-invariant (Valpha14i) NK T cells.
- To identify factors influencing iNKT cell ontogeny, particularly in males.
Main Methods:
- Analysis of Valpha14i NK T cell populations in genetically modified mouse models (B6.IFN-alphabetaR1-/-, B6.Tyk2-/-, B6.STAT1-/-, 129.IFN-alphabetaR1-/-, B6.IFN-alphabetaR1-/+).
- Assessment of CD1d1 levels and CD1d1-antigen presentation.
- Evaluation of sex-specific differences in iNKT cell development.
Main Results:
- Absence of Valpha14i NK T cells in male B6.IFN-alphabetaR1-/- mice, with normal conventional T and NK cell populations.
- The defect is intrinsic to male Valpha14i NK T cells and highly penetrant (>99%), while female mice are unaffected.
- The deficiency is Y-linked and independent of Interferon-alpha/beta signaling.
Conclusions:
- Y-linked genes exclusively influence Valpha14i NK T cell development in males.
- This study highlights the unique ontogeny of innate iNKT cells and identifies a novel sex-specific genetic regulation.
- Interferon signaling is not required for this aspect of iNKT cell development.
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