Cruz P D, Nixon-Fulton J, Tigelaar R E, Bergstresser P R
Department of Dermatology, University of Texas, Southwestern Medical Center, Dallas.
Photodermatol. 1988 Jun;5(3):126-32.
Exposure of mouse skin to UV radiation in doses comparable to those commonly received by humans has been shown to diminish the capacity of irradiated skin to mediate the induction of contact hypersensitivity to dinitrofluorobenzene (DNFB). In other studies, contact sensitization reactions to the structurally related hapten, trinitrochlorobenzene (TNCB), have been used to test the immunogenic properties of haptenated subpopulations of epidermal cells. To extend the applicability of TNCB to experiments that examine UVB modulation of immunization by epidermal cells, we examined the sensitivity of TNCB-induced contact hypersensitivity to low doses of UVB radiation. Abdominal skin of C3H mice was exposed to daily doses of 660 J/m2 broad-band UV radiation for 4 successive days. Immediately following the final exposure, 7% TNCB was applied to irradiated or non-irradiated skin of designated mice. After 5 days, mice were ear-challenged with 2% TNCB, and incremental ear-swelling responses were measured. Mice sensitized with TNCB through irradiated skin exhibited significantly diminished responses compared with UVB-treated mice sensitized through non-irradiated skin. We also found that mice initially sensitized with TNCB through irradiated skin but subsequently painted with oxazolone on normal skin developed full responses to ear-challenge with oxazolone. In contrast, mice sensitized initially with TNCB through irradiated skin failed to fully immunize even after TNCB was repainted on normal skin at a later date. We conclude that low-dose UVB radiation interrupts the induction of contact hypersensitivity to TNCB, leading to hapten-specific nonresponsiveness rather than hypersensitivity, and that this capacity to prevent successful immunization with TNCB is limited to the site of irradiation.(ABSTRACT TRUNCATED AT 250 WORDS)
已表明,将小鼠皮肤暴露于与人类通常接受剂量相当的紫外线辐射下,会降低受辐射皮肤介导对二硝基氟苯(DNFB)接触性超敏反应诱导的能力。在其他研究中,对结构相关的半抗原三硝基氯苯(TNCB)的接触致敏反应已被用于测试表皮细胞半抗原化亚群的免疫原性特性。为了将TNCB的适用性扩展到研究表皮细胞免疫的UVB调节的实验中,我们研究了TNCB诱导的接触性超敏反应对低剂量UVB辐射的敏感性。将C3H小鼠的腹部皮肤连续4天每天暴露于660 J/m²的宽带紫外线辐射。在最后一次暴露后立即将7%的TNCB应用于指定小鼠的受辐射或未受辐射皮肤。5天后,用2%的TNCB对小鼠耳部进行激发,并测量耳部肿胀的递增反应。与通过未受辐射皮肤致敏的UVB处理小鼠相比,通过受辐射皮肤用TNCB致敏的小鼠表现出明显减弱的反应。我们还发现,最初通过受辐射皮肤用TNCB致敏但随后在正常皮肤上涂抹恶唑酮的小鼠对恶唑酮耳部激发产生了完全反应。相比之下,最初通过受辐射皮肤用TNCB致敏的小鼠即使在后来在正常皮肤上重新涂抹TNCB后也未能完全免疫。我们得出结论,低剂量UVB辐射会中断对TNCB接触性超敏反应的诱导,导致半抗原特异性无反应性而非超敏反应,并且这种阻止用TNCB成功免疫的能力仅限于照射部位。(摘要截短至250字)