First Author | Kato-Nagaoka N | Year | 2015 |
Journal | Immunology | Volume | 146 |
Issue | 1 | Pages | 59-69 |
PubMed ID | 25967857 | Mgi Jnum | J:249672 |
Mgi Id | MGI:5922231 | Doi | 10.1111/imm.12480 |
Citation | Kato-Nagaoka N, et al. (2015) Enhanced differentiation of intraepithelial lymphocytes in the intestine of polymeric immunoglobulin receptor-deficient mice. Immunology 146(1):59-69 |
abstractText | To clarify the effect of secretory IgA (sIgA) deficiency on gut homeostasis, we examined intraepithelial lymphocytes (IELs) in the small intestine (SI) of polymeric immunoglobulin receptor-deficient (pIgR(-/-) ) mice. The pIgR(-/-) mice exhibited the accumulation of CD8alphabeta(+) T-cell receptor (TCR)-alphabeta(+) IELs (CD8alphabeta(+) alphabeta-IELs) after weaning, but no increase of CD8alphabeta(+) gammadelta-IELs was detected in pIgR(-/-) TCR-beta(-/-) mice compared with pIgR(+/+) TCR-beta(-/-) mice. When 5-bromo-2'-deoxyuridine (BrdU) was given for 14 days, the proportion of BrdU-labelled cells in SI-IELs was not different between pIgR(+/+) mice and pIgR(-/-) mice. However, the proportion of BrdU-labelled CD8alphabeta(+) -IELs became higher in pIgR(-/-) mice than pIgR(+/+) mice 10 days after discontinuing BrdU-labelling. Intravenously transferred splenic T cells migrated into the intraepithelial compartments of pIgR(+/+) TCR-beta(-/-) mice and pIgR(-/-) TCR-beta(-/-) mice to a similar extent. In contrast, in the case of injection of immature bone marrow cells, CD8alphabeta(+) alphabeta-IELs increased much more in the SI of pIgR(-/-) TCR-beta(-/-) mice than pIgR(+/+) TCR-beta(-/-) mice 8 weeks after the transfer. alphabeta-IELs from pIgR(-/-) mice could produce more interferon-gamma and interleukin-17 than those of pIgR(+/+) mice, and intestinal permeability tended to increase in the SI of pIgR(-/-) mice with aging. Taken together, these results indicate that activated CD8alphabeta(+) alphabeta-IELs preferentially accumulate in pIgR(-/-) mice through the enhanced differentiation of immature haematopoietic precursor cells, which may subsequently result in the disruption of epithelial integrity. |