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紫外线辐射对接触致敏剂免疫的局部影响。I. 将三硝基氯苯应用于紫外线照射的皮肤对接触性超敏反应的下调作用。

Local effects of UV radiation on immunization with contact sensitizers. I. Down-regulation of contact hypersensitivity by application of TNCB to UV-irradiated skin.

作者信息

Cruz P D, Nixon-Fulton J, Tigelaar R E, Bergstresser P R

机构信息

Department of Dermatology, University of Texas, Southwestern Medical Center, Dallas.

出版信息

Photodermatol. 1988 Jun;5(3):126-32.

PMID:3174491
Abstract

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)

摘要

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)

相似文献

1
Local effects of UV radiation on immunization with contact sensitizers. I. Down-regulation of contact hypersensitivity by application of TNCB to UV-irradiated skin.紫外线辐射对接触致敏剂免疫的局部影响。I. 将三硝基氯苯应用于紫外线照射的皮肤对接触性超敏反应的下调作用。
Photodermatol. 1988 Jun;5(3):126-32.
2
Local and systemic consequences of acute, low-dose ultraviolet B radiation are mediated by different immune regulatory mechanisms.急性低剂量紫外线B辐射的局部和全身影响是由不同的免疫调节机制介导的。
Eur J Immunol. 1994 Aug;24(8):1765-70. doi: 10.1002/eji.1830240807.
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Comparison of sensitizing protocols for ultraviolet B-induced immunosuppression in C3H mice.
Photodermatol Photoimmunol Photomed. 1994 Jun;10(3):106-10.
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Active induction of unresponsiveness (tolerance) to DNFB by in vivo ultraviolet-exposed epidermal cells is dependent upon infiltrating class II MHC+ CD11bbright monocytic/macrophagic cells.体内紫外线照射的表皮细胞对二硝基氟苯(DNFB)的无反应性(耐受性)的主动诱导依赖于浸润的II类主要组织相容性复合体(MHC)+ CD11b亮单核细胞/巨噬细胞。
J Immunol. 1994 Dec 1;153(11):4915-24.
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Polypodium leucotomos inhibits ultraviolet B radiation-induced immunosuppression.白叶铁线蕨抑制紫外线B辐射诱导的免疫抑制。
Photodermatol Photoimmunol Photomed. 2008 Jun;24(3):134-41. doi: 10.1111/j.1600-0781.2008.00352.x.
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Disparate effects of in vitro low-dose UVB irradiation on intravenous immunization with purified epidermal cell subpopulations for the induction of contact hypersensitivity.
J Invest Dermatol. 1989 Feb;92(2):160-5. doi: 10.1111/1523-1747.ep12276682.
7
Antigen-presenting activity of draining lymph node cells from mice painted with a contact allergen during ultraviolet carcinogenesis.紫外线致癌过程中接触性变应原涂抹小鼠引流淋巴结细胞的抗原呈递活性
J Immunol. 1991 Mar 15;146(6):1717-21.
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alpha-Melanocyte-stimulating hormone induces hapten-specific tolerance in mice.α-黑素细胞刺激素诱导小鼠产生半抗原特异性耐受性。
J Immunol. 1996 Jan 15;156(2):473-8.
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In vivo evidence that ultraviolet B-induced suppression of allergic contact sensitivity is associated with functional inactivation of Th1 cells.紫外线B诱导的过敏性接触敏感性抑制与Th1细胞功能失活相关的体内证据。
Photodermatol Photoimmunol Photomed. 1994 Oct;10(5):206-11.
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Establishment of an atopic dermatitis-like skin model in a hairless mouse by repeated elicitation of contact hypersensitivity that enables to conduct functional analyses of the stratum corneum with various non-invasive biophysical instruments.通过反复激发接触性超敏反应在无毛小鼠中建立特应性皮炎样皮肤模型,该模型能够使用各种非侵入性生物物理仪器对角质层进行功能分析。
Skin Res Technol. 2004 May;10(2):122-9. doi: 10.1111/j.1600-0846.2004.00062.x.

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Dissection of antigenic and irritative effects of epicutaneously applied haptens in mice. Evidence that not the antigenic component but nonspecific proinflammatory effects of haptens determine the concentration-dependent elicitation of allergic contact dermatitis.
表皮应用半抗原对小鼠的抗原性和刺激性作用剖析。证据表明,决定过敏性接触性皮炎浓度依赖性诱发的不是半抗原的抗原成分,而是其非特异性促炎作用。
J Clin Invest. 1996 Sep 1;98(5):1158-64. doi: 10.1172/JCI118899.
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Langerhans cells are initiators of the immunosuppressive effect of ultraviolet B radiation.朗格汉斯细胞是紫外线B辐射免疫抑制作用的启动者。
Springer Semin Immunopathol. 1992;13(3-4):281-8. doi: 10.1007/BF00200528.