Blockage of Th17 cells differentiation exacerbated mouse acute intestine graft-versus-host disease following allogeneic bone marrow transplantation / 中华血液学杂志
Chinese Journal of Hematology
; (12): 1024-1027, 2012.
Article
em Zh
| WPRIM
| ID: wpr-323499
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ABSTRACT
<p><b>OBJECTIVE</b>To study the role of Th17 cells in acute intestine graft-versus-host disease following allogenetic bone marrow transplantation(allo-BMT).</p><p><b>METHODS</b>Mice were split randomly into five groups: normal control, irradiated, allo-BMT, allo-BMT + DMSO and allo-BMT + Halofuginone (HF) groups. HF was given intraperitoneally at a dose of 5 µg per mouse from -1 d to 10 d after allo-BMT. aGVHD symptoms were followed-up to perform clinical and pathogenic scores. The levels of Th1/Th17, interleukin-17 and interferon-γ were measured by flow cytometry at day 7 d. mRNA expressions of T-bet, RORγT, CXCL9, CXCL10, CXCL11 and CCL20 in intestine were evaluated by real-time PCR.</p><p><b>RESULTS</b>Intestinal damages in allo-BMT-HF mice was more serious than in normal control and allo-BMT groups at day 14 after transplantation. At day 7, Th17 ratio in allo-BMT + HF group was significantly lower than in allo-BMT group. IL-17A was not detected, but Th1 ratio was higher in allo-BMT + HF. There was a similar increment in the relative expressions of T-bet in both allo-BMT and allo-BMT + HF groups. Expressions of CXCL9 and CXCL10 elevated in allo-BMT + HF group, which were significantly higher than those in allo-BMT group (P < 0.01). CCL20 expression significantly increased in allo-BMT group, but it was not detected in allo-BMT + HF group.</p><p><b>CONCLUSION</b>Blockage of th17 cells differentiation exacerbated acute intestine graft versus-host disease.</p>
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Assunto principal:
Patologia
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Transplante Homólogo
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Diferenciação Celular
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Transplante de Medula Óssea
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Biologia Celular
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Células Th17
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Doença Enxerto-Hospedeiro
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Enteropatias
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Intestinos
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Camundongos Endogâmicos BALB C
Limite:
Animals
Idioma:
Zh
Revista:
Chinese Journal of Hematology
Ano de publicação:
2012
Tipo de documento:
Article