The late phase skin reaction: evidence for activation of the coagulation system in an IgE-dependent reaction in man.

The late phase skin reaction: evidence for activation of the coagulation system in an IgE-dependent reaction in man.
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晚期皮肤反应:人类 IgE 依赖性反应中凝血系统激活的证据。

DOI:
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发表时间:
1979
影响因子:
4.4
通讯作者:
R. W. Davis
R. W. Davis
中科院分区:
医学2区
文献类型:
--
作者:
R. deShazo;A. Levinson;H. Dvorak;R. W. Davis

文献摘要

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晚相反应(LPR),一个IgE依赖性的后遗症风团和耀斑反应(WFR),研究了豚草(RW)敏感的受试者15分钟和6至8小时后,皮内注射RW。通过皮肤试验滴定至LPR消退,确定WFR在LPR发生中的作用以及LPR对RW剂量的依赖性。LPR大小与WFR大小相关。观察到LPR,WFR小至9.5 ± 1.0 mm(S.E.M.)。RW剂量小至0.01蛋白氮单位(PNU)。在一组WFR阳性但LPR阴性的受试者中,尽管通过同时注射RW +组胺(RW-H)将WFR增加至18.2 ± 1.3 mm,但未诱导LPR。直接和Prausnitz-Kustner(P-K)LPR的1 µm活检切片的光学显微镜检查显示,混合细胞浸润与分离WFR后6小时观察到的浸润在性质上没有差异。在免疫球蛋白或补体的情况下,通过荧光显微镜在LPR中观察到纤维蛋白沉积,但在对照组中未观察到。 这些数据表明,LPR可能遵循小RW剂量。此外,RW-H注入诱导LPR的失败反对WFR在LPR的发生中的看门人作用。尽管纤维蛋白沉积解释了LPR的临床硬结,但细胞浸润的意义尚不清楚。这种纤维蛋白沉积是这些IgE依赖性“时间延迟”反应中凝血系统激活的证据。
The late phase reaction (LPR), an IgE-dependent sequel to the wheal and flare response (WFR), was studied in ragweed (RW)-sensitive subjects 15 min and 6 to 8 hr after intradermal RW injection. The role of WFR in the genesis of LPR and LPR dependence on RW dose were determined by skin test titration to extinction of LPR. LPR size correlated with WFR size. LPR were noted with WFR as small as 9.5 ± 1.0 mm (S.E.M.) and RW doses as small as 0.01 protein nitrogen unit (PNU). In a group of WFR-positive but LPR-negative subjects, LPR were not induced despite increasing WFR to 18.2 ± 1.3 mm by simultaneous injection of RW + histamine (RW-H). Light microscopy of 1-µm biopsy sections of direct and Prausnitz-Kustner (P-K) LPR revealed a mixed cellular infiltrate qualitatively no different than that seen 6 hr after isolated WFR. Fibrin deposition in the absence of immunoglobulin or complement was seen by fluorescent microscopy in LPR but not in controls. These data suggest that LPR may follow small RW doses. Furthermore, the failure of RW-H injection to induce LPR argues against a gatekeeper role for WFR in the genesis of LPR. The significance of the cellular infiltrate is not clear although fibrin deposition explains the clinical induration of LPR. This fibrin deposition is evidence for activation of the coagulation system in these IgE-dependent “delayed in time” reactions.