Jun B D, Law M Y, Daynes R A, Roberts L K
Department of Anatomy, Chonbuk National University Medical School, Chonju, Republic of Korea.
Reg Immunol. 1989 Jul-Aug;2(4):225-35.
The density of Langerhans cells (LC) is significantly decreased in skin sites exposed to ultraviolet radiation (UVR). This results in reduced antigen-presenting cell (APC) activity in UVR-exposed skin. We have previously reported that the recovery in the density of ATPase/Ia+ epidermal cells (EC) parallels the restoration of APC function in the UVR-exposed skin of mice. The present study was designed to determine whether the spleen might serve as a source of ATPase/Ia+ cells to restore APC function to the skin after UVR exposure. ATPase/Ia+ EC densities were calculated from skin biopsies taken from BALB/c mice at various time points after low dose UVR treatment (2000 J/m2 protracted over 4 days). The recovery rate of ATPase/Ia+ EC in splenectomized mice after UVR exposure was similar, although delayed, compared to that of sham-operated mice. For example, 3 days after UVR exposure the density of ATPase/Ia+ EC in sham controls was 90% of normal and exceeded normal values by 5 days. In contrast, ATPase/Ia+ EC density in splenectomized mice was 60% of normal at 3 days and did not exceed normal values until 7 days after UVR exposure. Normal recovery of ATPase/Ia+ EC was restored to splenectomized mice given an adoptive transfer of syngeneic spleen cells immediately after UVR exposure. Fluorescein-labeled spleen cells used for adoptive transfer were observed within the epidermis of splenectomized mice 1 and 3 days after UVR exposure. Indirect immunofluorescent staining employing phycoerythrin-labeled reagents revealed that the fluorescein-labeled splenic EC expressed Ia, MAC-1, CLA, and Fc-receptor molecules. These results indicate that a portion of the ATPase/Ia+ EC that recovery after UVR exposure originate from the spleen. These cells may be distinct from LC, but appear to restore APC function to the skin following LC depletion by UVR exposure.
在暴露于紫外线辐射（UVR）的皮肤部位，朗格汉斯细胞（LC）的密度显著降低。这导致暴露于UVR的皮肤中抗原呈递细胞（APC）的活性降低。我们之前曾报道，ATP酶/Ia+表皮细胞（EC）密度的恢复与UVR照射后小鼠皮肤中APC功能的恢复同步。本研究旨在确定脾脏是否可能作为ATP酶/Ia+细胞的来源，在UVR照射后恢复皮肤的APC功能。在低剂量UVR治疗（2000 J/m2，持续4天）后的不同时间点，从BALB/c小鼠身上取皮肤活检组织，计算ATP酶/Ia+ EC密度。与假手术小鼠相比，脾切除小鼠在UVR照射后的ATP酶/Ia+ EC恢复率相似，尽管有所延迟。例如，UVR照射后3天，假手术对照组中ATP酶/Ia+ EC的密度为正常水平的90%，并在5天后超过正常值。相比之下，脾切除小鼠在UVR照射后3天，ATP酶/Ia+ EC密度为正常水平的60%，直到照射后7天才超过正常值。在UVR照射后立即对脾切除小鼠进行同基因脾细胞的过继转移，可使ATP酶/Ia+ EC恢复正常恢复。在UVR照射后1天和3天，在脾切除小鼠的表皮内观察到用于过继转移的荧光素标记的脾细胞。采用藻红蛋白标记试剂的间接免疫荧光染色显示，荧光素标记的脾EC表达Ia、MAC-1、CLA和Fc受体分子。这些结果表明，UVR照射后恢复的部分ATP酶/Ia+ EC来源于脾脏。这些细胞可能与LC不同，但在UVR照射导致LC耗竭后，似乎能恢复皮肤的APC功能。
