Novel loci controlling lymphocyte proliferative response to cytokines and their clustering with loci controlling autoimmune reactions, macrophage function and lung tumor susceptibility
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
15551356
DOI
10.1002/ijc.20731
Knihovny.cz E-zdroje
- MeSH
- autoimunita imunologie MeSH
- cytokiny farmakologie MeSH
- genetická predispozice k nemoci MeSH
- genom MeSH
- genotyp MeSH
- lokus kvantitativního znaku * MeSH
- lymfocyty fyziologie MeSH
- makrofágy fyziologie MeSH
- myši MeSH
- nádorová transformace buněk MeSH
- nádory plic etiologie genetika imunologie MeSH
- proliferace buněk MeSH
- zánět * MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- myši MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- cytokiny MeSH
Novel genotyping and statistical tools have led to mapping of numerous QTL loci for multigenic traits that previously could not be detected. The relationships of these QTL families to other QTL families and the functional specialization of their members can now be studied. We have mapped a number of loci controlling activation of T lymphocytes by mitogens and cytokines and their capacity to produce cytokines. In (O20xOcB-9)F2 hybrids, we mapped 3 novel loci controlling proliferative T-cell response to cytokines IL-2 and IL-4 (Cinda3) or IL-4 only (Cinda4 and Cinda5). OcB-9 allele at Cinda3 controls a higher response than the O20 allele to both IL-2 and IL-4, and OcB-9 alleles of Cinda4 and Cinda5 control higher response to IL-4. These novel Cinda loci and the previously mapped Cinda1 locus seem to be located in genomic regions together with other QTL families: macrophage function loci Marif1 and Marif2, proteoglycan-induced arthritis loci Pgia4, Pgia7 and Pgia12 and lung tumor susceptibility loci Sluc1, Sluc4, Sluc6 and Sluc20. The possible relevance of these QTL associations in several different sites of the genome for the immune response, inflammation and tumorigenesis has to be elucidated.
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