Y Chromosome–Linked B and NK Cell Deficiency in Mice (original) (raw)
Journal Article
Department of Microbiology and Immunology, Tohoku University Graduate School of Medicine
, Sendai 980-8575,
Japan
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Department of Microbiology and Immunology, Tohoku University Graduate School of Medicine
, Sendai 980-8575,
Japan
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Department of Biochemistry, Tohoku University Graduate School of Medicine
, Sendai 980-8575,
Japan
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Department of Microbiology and Immunology, Tohoku University Graduate School of Medicine
, Sendai 980-8575,
Japan
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Department of Microbiology and Immunology, Tohoku University Graduate School of Medicine
, Sendai 980-8575,
Japan
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Central Institute for Experimental Animals
, Kawasaki 210-0821,
Japan
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Department of Microbiology and Immunology, Tohoku University Graduate School of Medicine
, Sendai 980-8575,
Japan
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Department of Cell Proliferation, Tohoku University Graduate School of Medicine
, Sendai 980-8575,
Japan
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Department of Immunology, Toho University School of Medicine
, Tokyo 143-8540,
Japan
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Department of Human Genetics, Yokohama City University Graduate School of Medicine
, Yokohama 236-0004,
Japan
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Received:
31 January 2013
Cite
Shu-lan Sun, Satoshi Horino, Ari Itoh-Nakadai, Takeshi Kawabe, Atsuko Asao, Takeshi Takahashi, Takanori So, Ryo Funayama, Motonari Kondo, Hirotomo Saitsu, Naomichi Matsumoto, Keiko Nakayama, Naoto Ishii, Y Chromosome–Linked B and NK Cell Deficiency in Mice, The Journal of Immunology, Volume 190, Issue 12, June 2013, Pages 6209–6220, https://doi.org/10.4049/jimmunol.1300303
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Abstract
There are no primary immunodeficiency diseases linked to the Y chromosome, because the Y chromosome does not contain any vital genes. We have established a novel mouse strain in which all males lack B and NK cells and have Peyer’s patch defects. By 10 wk of age, 100% of the males had evident immunodeficiencies. Mating these immunodeficient males with wild-type females on two different genetic backgrounds for several generations demonstrated that the immunodeficiency is linked to the Y chromosome and is inherited in a Mendelian fashion. Although multicolor fluorescence in situ hybridization analysis showed that the Y chromosome in the mutant male mice was one third shorter than that in wild-type males, exome sequencing did not identify any significant gene mutations. The precise molecular mechanisms are still unknown. Bone marrow chimeric analyses demonstrated that an intrinsic abnormality in bone marrow hematopoietic cells causes the B and NK cell defects. Interestingly, fetal liver cells transplanted from the mutant male mice reconstituted B and NK cells in lymphocyte-deficient Il2rg−/− recipient mice, whereas adult bone marrow transplants did not. Transducing the EBF gene, a master transcription factor for B cell development, into mutant hematopoietic progenitor cells rescued B cell but not NK cell development both in vitro and in vivo. These Y chromosome–linked immunodeficient mice, which have preferential B and NK cell defects, may be a useful model of lymphocyte development.
Copyright © 2013 by The American Association of Immunologists, Inc.
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