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Article: Cutting edge: LFA-1 is required for liver NK1.1+TCRαβ+ cell development evidence that liver NK1.1+TCRαβ+ cells originate from multiple pathways

TitleCutting edge: LFA-1 is required for liver NK1.1<sup>+</sup>TCRαβ<sup>+</sup> cell development evidence that liver NK1.1<sup>+</sup>TCRαβ<sup>+</sup> cells originate from multiple pathways
Authors
Issue Date1999
Citation
Journal of Immunology, 1999, v. 162, n. 7, p. 3753-3756 How to Cite?
AbstractUsing mice deficient for LFA-1, CD44, and ICAM-1, we examined the role of these adhesion molecules in NK1.1+TCRαβ+ (NKT) cell development. Although no defect in NKT cell development was observed in CD44(-/-) and ICAM-1(-/-) mice, a dramatic reduction of liver NKT cells was observed in LFA-1(-/-) mice. Normal numbers of NKT cells were present in other lymphoid organs in LFA-1(-/-) mice. When LFA-1(-/-) splenocytes were injected i.v. into wild-type mice, the frequency of NKT cells among donor-derived cells in the recipient liver was normal. In contrast, when LFA-1(-/-) bone marrow (BM) cells were injected i.v. into irradiated wild-type mice, the frequency of liver NKT cells was significantly lower than that of mice injected with wild- type BM cells. Collectively, these data indicate that LFA-1 is required for the development of liver NKT cells, rather than the migration to and/or subsequent establishment of mature NKT cells in the liver.
Persistent Identifierhttp://hdl.handle.net/10722/291488
ISSN
2021 Impact Factor: 5.426
2020 SCImago Journal Rankings: 2.737
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorOhteki, Toshiaki-
dc.contributor.authorMaki, Chikako-
dc.contributor.authorKoyasu, Shigeo-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorOhashi, Pamela S.-
dc.date.accessioned2020-11-17T14:54:28Z-
dc.date.available2020-11-17T14:54:28Z-
dc.date.issued1999-
dc.identifier.citationJournal of Immunology, 1999, v. 162, n. 7, p. 3753-3756-
dc.identifier.issn0022-1767-
dc.identifier.urihttp://hdl.handle.net/10722/291488-
dc.description.abstractUsing mice deficient for LFA-1, CD44, and ICAM-1, we examined the role of these adhesion molecules in NK1.1+TCRαβ+ (NKT) cell development. Although no defect in NKT cell development was observed in CD44(-/-) and ICAM-1(-/-) mice, a dramatic reduction of liver NKT cells was observed in LFA-1(-/-) mice. Normal numbers of NKT cells were present in other lymphoid organs in LFA-1(-/-) mice. When LFA-1(-/-) splenocytes were injected i.v. into wild-type mice, the frequency of NKT cells among donor-derived cells in the recipient liver was normal. In contrast, when LFA-1(-/-) bone marrow (BM) cells were injected i.v. into irradiated wild-type mice, the frequency of liver NKT cells was significantly lower than that of mice injected with wild- type BM cells. Collectively, these data indicate that LFA-1 is required for the development of liver NKT cells, rather than the migration to and/or subsequent establishment of mature NKT cells in the liver.-
dc.languageeng-
dc.relation.ispartofJournal of Immunology-
dc.titleCutting edge: LFA-1 is required for liver NK1.1<sup>+</sup>TCRαβ<sup>+</sup> cell development evidence that liver NK1.1<sup>+</sup>TCRαβ<sup>+</sup> cells originate from multiple pathways-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.pmid10201888-
dc.identifier.scopuseid_2-s2.0-0033120557-
dc.identifier.volume162-
dc.identifier.issue7-
dc.identifier.spage3753-
dc.identifier.epage3756-
dc.identifier.isiWOS:000079278000002-
dc.identifier.issnl0022-1767-

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