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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
Title | Cutting 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 |
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Authors | |
Issue Date | 1999 |
Citation | Journal of Immunology, 1999, v. 162, n. 7, p. 3753-3756 How to Cite? |
Abstract | Using 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 Identifier | http://hdl.handle.net/10722/291488 |
ISSN | 2023 Impact Factor: 3.6 2023 SCImago Journal Rankings: 1.558 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Ohteki, Toshiaki | - |
dc.contributor.author | Maki, Chikako | - |
dc.contributor.author | Koyasu, Shigeo | - |
dc.contributor.author | Mak, Tak W. | - |
dc.contributor.author | Ohashi, Pamela S. | - |
dc.date.accessioned | 2020-11-17T14:54:28Z | - |
dc.date.available | 2020-11-17T14:54:28Z | - |
dc.date.issued | 1999 | - |
dc.identifier.citation | Journal of Immunology, 1999, v. 162, n. 7, p. 3753-3756 | - |
dc.identifier.issn | 0022-1767 | - |
dc.identifier.uri | http://hdl.handle.net/10722/291488 | - |
dc.description.abstract | Using 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.language | eng | - |
dc.relation.ispartof | Journal of Immunology | - |
dc.title | Cutting 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.type | Article | - |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.pmid | 10201888 | - |
dc.identifier.scopus | eid_2-s2.0-0033120557 | - |
dc.identifier.volume | 162 | - |
dc.identifier.issue | 7 | - |
dc.identifier.spage | 3753 | - |
dc.identifier.epage | 3756 | - |
dc.identifier.isi | WOS:000079278000002 | - |
dc.identifier.issnl | 0022-1767 | - |