title: Attenuation of migration properties of CD4+ T cells from aged mice correlates with decrease in chemokine receptor expression, response to retinoic acid, and RALDH expression compared to young mice.
abstract: Aging results in attenuation of abilities to mount appropriate immune responses. The influence of aging on CD4(+) T cell migration ability toward chemokines was investigated with young and aged mice. We found functional decline in migration ability toward CCL19 and also decreased CCR7 expression level in antigen-stimulated CD4(+) T cells from aged mice compared with those from young mice. Upon addition of retinoic acid (RA), CD4(+) T cells from aged mice showed decreased CCR9 expression level compared to young mice and the migration ability of CD4(+) T cells from aged mice toward CCL25 was attenuated compared to young mice. We also observed that the expression of RALDH2 mRNA was decreased in mesenteric lymph node dendritic cells from aged mice compared to those from young mice. These results demonstrate that attenuated migration abilities of CD4(+) T cells were observed in aged mice, which correlated with decreased chemokine receptor expression. Furthermore, the reduced production and response to RA by aging may be one of the causes of such attenuated migration abilities in the intestinal immune system.
authors.affiliation: a Research Center for Food Safety, Graduate School of Agricultural and Life Sciences , The University of Tokyo , Tokyo , Japan.
authors.forename: Jihyun
authors.initials: J
authors.lastname: Park
authors.forename: Takuya
authors.initials: T
authors.lastname: Miyakawa
authors.forename: Aya
authors.initials: A
authors.lastname: Shiokawa
authors.forename: Haruyo
authors.initials: H
authors.lastname: Nakajima-Adachi
authors.forename: Masaru
authors.initials: M
authors.lastname: Tanokura
authors.forename: Satoshi
authors.initials: S
authors.lastname: Hachimura
mesh_terms: D000375:Aging / Q000378:metabolism*; D000080924:Aldehyde Dehydrogenase 1 Family; D000445:Aldehyde Oxidoreductases / Q000235:genetics*; D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000166:cytology* / Q000187:drug effects; D002465:Cell Movement / Q000187:drug effects*; D054415:Chemokine CCL19 / Q000378:metabolism; D019742:Chemokines, CC / Q000378:metabolism; D005260:Female; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects*; D016023:Integrins / Q000378:metabolism; D007527:Isoenzymes / Q000235:genetics; D051379:Mice; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D054388:Receptors, CCR / Q000378:metabolism; D054400:Receptors, CCR7 / Q000378:metabolism; D019707:Receptors, Chemokine / Q000378:metabolism*; D050697:Retinal Dehydrogenase / Q000235:genetics; D013154:Spleen / Q000276:immunology; D014212:Tretinoin / Q000494:pharmacology*
chemical_list: C119309:CC chemokine receptor 9; C491541:Ccl25 protein, mouse; D054415:Chemokine CCL19; D019742:Chemokines, CC; D016023:Integrins; D007527:Isoenzymes; D012333:RNA, Messenger; D054388:Receptors, CCR; D054400:Receptors, CCR7; D019707:Receptors, Chemokine; C071777:integrin alpha4beta7; D014212:Tretinoin; D000445:Aldehyde Oxidoreductases; D000080924:Aldehyde Dehydrogenase 1 Family; C515028:ALDH1A1 protein, mouse; C470579:RALDH2 protein, mouse; D050697:Retinal Dehydrogenase
keywords: T cell; aging; migration