Niizeki H, Alard P, Streilein J W
Schepens Eye Research Institute and Department of Dermatology, Harvard Medical School, Boston, MA 02114, USA.
J Immunol. 1997 Dec 1;159(11):5183-6.
Since nerve termini on Langerhans cells (LC) contain calcitonin gene-related peptide (CGRP), and since ultraviolet B radiation (UVR) causes CGRP to be released from cutaneous nerve endings, we examined whether CGRP participates in the immune aberrations caused in skin by UVR. First, intradermally injected CGRP, in a dose-dependent manner, reduced LC density and impaired CH induction when hapten was painted on the injected site. Second, CGRP antagonist restored CH induction after UVR. Third, anti-TNF-alpha Abs injected before CGRP prevented the loss of LC density and restored CH induction. Fourth, CGRP failed to impair CH induction in mast cell-deficient mice. Fifth, CGRP induced mast cells to release TNF-alpha. We conclude that CGRP plays an essential role in the loss of CH induction after UVR. These data indicate that UVR, by causing the release of CGRP from cutaneous nerve endings, triggers mast cell release of TNF-alpha, which impairs CH induction.
由于朗格汉斯细胞（LC）上的神经末梢含有降钙素基因相关肽（CGRP），且紫外线B辐射（UVR）会使CGRP从皮肤神经末梢释放，因此我们研究了CGRP是否参与UVR在皮肤中引起的免疫异常。首先，皮内注射CGRP以剂量依赖的方式降低了LC密度，并在注射部位涂抹半抗原时损害了迟发型超敏反应（CH）的诱导。其次，CGRP拮抗剂在UVR后恢复了CH诱导。第三，在注射CGRP之前注射抗TNF-α抗体可防止LC密度的降低并恢复CH诱导。第四，CGRP未能损害肥大细胞缺陷小鼠的CH诱导。第五，CGRP诱导肥大细胞释放TNF-α。我们得出结论，CGRP在UVR后迟发型超敏反应诱导的丧失中起重要作用。这些数据表明，UVR通过导致CGRP从皮肤神经末梢释放，触发肥大细胞释放TNF-α，从而损害迟发型超敏反应诱导。
