title: Impairment of hepatic NK cell development in IFN-γ deficient mice.
abstract: It is already clearly demonstrated that IFN-γ plays important roles in differentiation and maturation of T cells, B cells and macrophages; however, it is not clear whether NK cell development is regulated by IFN-γ. In our study by using IFN-γ-deficient mice (GKO), we observed that the percentage and number of NK1.1(+)CD3(-) cells were declined significantly in the liver, but not in the spleen, bone marrow and lymph node, of adult IFN-γ(-/-) mice. However, Lin(-)CD122(+) NK progenitor cells developed normally both in liver and bone marrow in IFN-γ(-/-) mice. Moreover, more mature CD27(-)CD11b(+) NK cells accumulated in the liver of IFN-γ(-/-) mice. Deficiency of IFN-γ resulted in the lower expression of CD69, GranzymeB and TRAIL by hepatic NK1.1(+)CD3(-) cells and the phenotypes of IFN-γ(-/-) hepatic NK1.1(+)CD3(-) cells were altered from WT hepatic NK cells. When stimulated with Poly (I:C) in vivo, attenuated accumulating in the liver and weaker expression of GranzymeB, TRAIL and FasL of NK1.1(+)CD3(-) cells were observed of IFN-γ(-/-) mice. Accordingly, these results demonstrate that IFN-γ plays important role in mounting liver environment for development of hepatic NK cells.
authors.affiliation: Institute of Immunology, Hefei National Laboratory for Physical Sciences at Microscale and School of Life Sciences, University of Science and Technology of China, Hefei 230027, China.
authors.forename: Xian
authors.initials: X
authors.lastname: Wu
authors.forename: Yongyan
authors.initials: Y
authors.lastname: Chen
authors.forename: Rui
authors.initials: R
authors.lastname: Sun
authors.forename: Haiming
authors.initials: H
authors.lastname: Wei
authors.forename: Zhigang
authors.initials: Z
authors.lastname: Tian
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000096:biosynthesis; D000945:Antigens, Differentiation, T-Lymphocyte / Q000096:biosynthesis; D001854:Bone Marrow Cells; D017252:CD3 Complex / Q000096:biosynthesis; D002454:Cell Differentiation; D003602:Cytotoxicity, Immunologic; D053804:Granzymes / Q000096:biosynthesis; D007371:Interferon-gamma / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D053646:Interleukin-2 Receptor beta Subunit / Q000378:metabolism; D007694:Killer Cells, Natural / Q000276:immunology / Q000502:physiology*; D037181:Lectins, C-Type / Q000096:biosynthesis; D008099:Liver / Q000166:cytology / Q000276:immunology*; D008198:Lymph Nodes / Q000166:cytology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D011070:Poly I-C / Q000494:pharmacology; D013154:Spleen / Q000166:cytology; D053221:TNF-Related Apoptosis-Inducing Ligand / Q000096:biosynthesis; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D017252:CD3 Complex; D053804:Granzymes; D007371:Interferon-gamma; D053646:Interleukin-2 Receptor beta Subunit; D037181:Lectins, C-Type; D011070:Poly I-C; D053221:TNF-Related Apoptosis-Inducing Ligand; D000099192:CD69 Antigens; C505654:Tnfsf10 protein, mouse; C509214:Gzmb protein, mouse