Prevention of airway allograft tolerance by polyinosinic:polycytidylic acid requires type I interferon responsiveness for mouse airway obliteration.
Prevention of airway allograft tolerance by polyinosinic:polycytidylic acid requires type I interferon responsiveness for mouse airway obliteration.
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通过聚肌苷：聚胞苷酸预防气道同种异体移植耐受需要 I 型干扰素对小鼠气道闭塞的反应性。
DOI：
10.1016/j.healun.2013.06.017
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发表时间：
2013
期刊：
影响因子：
--
通讯作者：
McDyer,JohnF
中科院分区：
文献类型：
--
作者：
Miller,HannahL;Shah,PaliD;Orens,JonathanB;McDyer,JohnF
呼吸道RNA病毒与肺移植受者（LTRS）中的闭塞性细支气管炎综合征（BOS）有关，然而调节气道闭塞的免疫机制仍不完全清楚。（聚肌苷酸：聚胞苷酸;聚（I：C）），病毒dsRNA的合成类似物，在消除供体特异性输血（DST）和抗CD 154单克隆抗体治疗建立的气道同种异体移植物耐受中，c气道移植物显示移植物内CD 8 + T细胞显著减少，同种异体特异性IFN-γ和TNF-α分泌显著受损，与活化表型和增殖证据脱钩。给DST/抗CD 154治疗的受体施用poly（I：C）使OAD病理学和CD 8+同种效应物应答恢复至未治疗小鼠中观察到的水平。然而，B6 IFNαβR−/−受体对poly（I：C）介导的耐受消除具有抗性，并且未发生CD 8+同种效应物应答或OAD。此外，单独将WT CD 8 + T细胞或CD 11 c+树突状细胞（DC）过继转移到用poly（I：C）和DST/抗CD 154处理的B6 IFNαβR−/−受体中不能消除气道移植物耐受性。结论总之，这些数据表明，通过dsRNA消除DST/抗CD 154诱导的气道同种异体移植物耐受性需要I型IFN对小鼠气道闭塞的反应性。
BACKGROUNDRespiratory RNA viruses are associated with bronchiolitis obliterans syndrome (BOS) in lung transplant recipients (LTRS), however the immune mechanisms that regulate airway obliteration remain incompletely understood.METHODSUsing the mouse heterotopic tracheal transplant (HTT) model of obliterative airway disease (OAD), we studied the role of dsRNA using (polyinosinic:polycytidylic acid; poly(I:C)), a synthetic analog of viral dsRNA, in abrogating airway allograft tolerance established with donor-specific transfusion (DST) and anti-CD154 mAb therapy.RESULTSWild-type (WT) B6 recipients of accepted BALB/c airway grafts demonstrated significantly reduced intragraft CD8+ T-cells with markedly impaired allospecific IFN-γ and TNF-α secretion, uncoupled from an activated phenotype and evidence of proliferation. Administration of poly(I:C) to DST/anti-CD154-treated recipients restored OAD pathology and CD8+ alloeffector responses to levels observed in untreated mice. However, B6 IFNαβR−/− recipients were resistant to the abrogation of tolerance mediated by poly(I:C) and did not develop CD8+ alloeffector responses or OAD. Further, adoptive transfers of either WT CD8+ T-cells or CD11c+ dendritic cells (DC) alone into B6 IFNαβR−/− recipients treated with poly(I:C) and DST/anti-CD154 were incapable of abrogating airway graft tolerance.CONCLUSIONSTogether, these data indicate abrogation of DST/anti-CD154-induced airway allograft tolerance via dsRNA requires type-I IFN responsiveness for mouse airway obliteration.
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DOI：
10.1165/rcmb.2007-0257rc
发表时间：
2007-12-01
影响因子：
6.4
作者：
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影响因子：
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发表时间：
2005-05
期刊：
The Journal of clinical investigation
影响因子：
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影响因子：
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DOI：
10.1084/jem.189.5.821
发表时间：
1999-03-01
期刊：
The Journal of experimental medicine
影响因子：
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Lanzavecchia A