A profound deficiency in thymic progenitor cells in mice lacking Jak3
| dc.contributor.author | Baird, Allison Michelle | |
| dc.contributor.author | Lucas, Julie Ann | |
| dc.contributor.author | Berg, Leslie J. | |
| dc.date | 2022-08-11T08:09:00.000 | |
| dc.date.accessioned | 2022-08-23T16:15:11Z | |
| dc.date.available | 2022-08-23T16:15:11Z | |
| dc.date.issued | 2000-10-18 | |
| dc.date.submitted | 2008-07-07 | |
| dc.identifier.citation | <p>J Immunol. 2000 Oct 1;165(7):3680-8.</p> | |
| dc.identifier.issn | 0022-1767 (Print) | |
| dc.identifier.doi | 10.4049/jimmunol.165.7.3680 | |
| dc.identifier.pmid | 11034372 | |
| dc.identifier.uri | http://hdl.handle.net/20.500.14038/34029 | |
| dc.description.abstract | Humans and mice with genetic deficiencies that lead to loss of signaling through common gamma-chain (gammac)-containing cytokine receptors have severe defects in B and T lymphocytes. In humans, these deficiencies lead to a complete absence of T cells, whereas in mice, small thymuses give rise to normal numbers of peripheral T cells. We have examined the first wave of developing T cells in Jak3-/-, IL-7-/-, and IL-7Ralpha-/- fetal mice, and have found a near absence of thymic progenitor cells. This deficiency is highlighted by the complete inability of Jak3-/- progenitor cells to reconstitute T cell development in the presence of competing wild-type cells. These data clearly demonstrate a strong common basis for the T cell deficiencies in mice and humans lacking gammac/Jak3 signaling pathways. | |
| dc.language.iso | en_US | |
| dc.relation | <p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11034372&dopt=Abstract ">Link to article in PubMed</a></p> | |
| dc.relation.url | https://doi.org/10.4049/jimmunol.165.7.3680 | |
| dc.subject | Animals; Apoptosis; Bone Marrow Transplantation; Cell Differentiation; Embryonic and Fetal Development; Female; Gene Expression Regulation, Developmental; Injections, Intralymphatic; Janus Kinase 3; Kinetics; Lymphopenia; Male; Mice; Mice, Congenic; Mice, Inbred C57BL; Mice, Knockout; Protein-Tyrosine Kinases; Signal Transduction; Stem Cells; Thymus Gland | |
| dc.subject | Life Sciences | |
| dc.subject | Medicine and Health Sciences | |
| dc.title | A profound deficiency in thymic progenitor cells in mice lacking Jak3 | |
| dc.type | Journal Article | |
| dc.source.journaltitle | Journal of immunology (Baltimore, Md. : 1950) | |
| dc.source.volume | 165 | |
| dc.source.issue | 7 | |
| dc.identifier.legacycoverpage | https://escholarship.umassmed.edu/gsbs_sp/68 | |
| dc.identifier.contextkey | 543961 | |
| html.description.abstract | <p>Humans and mice with genetic deficiencies that lead to loss of signaling through common gamma-chain (gammac)-containing cytokine receptors have severe defects in B and T lymphocytes. In humans, these deficiencies lead to a complete absence of T cells, whereas in mice, small thymuses give rise to normal numbers of peripheral T cells. We have examined the first wave of developing T cells in Jak3-/-, IL-7-/-, and IL-7Ralpha-/- fetal mice, and have found a near absence of thymic progenitor cells. This deficiency is highlighted by the complete inability of Jak3-/- progenitor cells to reconstitute T cell development in the presence of competing wild-type cells. These data clearly demonstrate a strong common basis for the T cell deficiencies in mice and humans lacking gammac/Jak3 signaling pathways.</p> | |
| dc.identifier.submissionpath | gsbs_sp/68 | |
| dc.contributor.department | Department of Pathology | |
| dc.contributor.department | Graduate School of Biomedical Sciences | |
| dc.source.pages | 3680-8 |