Action spectra of lupus erythematosus and experimental immunofluorescence

Cripps, D. J.

doi:10.1001/archderm.107.4.563

Cited by 51 publications

(33 citation statements)

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“…In addition, the patients with subacute cutaneous LE had persistence of erythema at 1 MED and frequently developed cutaneous LE in the irradiated test site (8). Cripps and Rankin also studied MEDs in LE patients and determined that the action spectrum of LE extends to the UVA range (11). Erythema at test sites persisted with exposures up to 330 nm.…”

Section: Discussionmentioning

confidence: 99%

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Photoexacerbation of cutaneous lupus erythematosus due to ultraviolet a emissions from a photocopier

Klein

Elmets

Callen

1995

Arthritis & Rheumatism

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This report describes a woman with systemic lupus erythematosus (LE) who worked as a photocopy technician and developed cutaneous LE of the hands, neck, face, and chest. Her skin lesions improved when she discontinued her employment. Testing of several photocopy devices showed emission of small quantities of ultraviolet A (UVA), but no UVB. Phototesting of the patient with UVA and UVB induced skin lesions that were clinically and histopathologically consistent with LE. Thus, the action spectrum of cutaneous LE may be within the UVB range, the UVA range, or both ranges of the solar spectrum, and repeated exposure to short bursts of light may induce clinical disease. This case suggests that occupational sources of UV light should be considered as possible exacerbating factors in LE.The role of sunlight in the induction and exacerbation of systemic and cutaneous lupus erythematosus (LE) is well documented (1). Skin lesions occur preferentially on sun-exposed skin, and photosensitivity is included as 1 of the 11 American College of Rheumatology (formerly, the American Rheumatism Association) criteria for the diagnosis of systemic LE (SLE) (2). Lesions of cutaneous LE can be induced by artificial, as well as natural, sources of ultraviolet (UV) light (3-1 1). However, the action spectrum of light of LE was originally thought to be limited to the UVB range (280-320 nm) ( 4 4 8 ) .Cutaneous L E lesions, which on physical examination have the appearance of persistent erythem- (12)(13)(14). Fluorescent lamps emit radiation in the UVA as well as the UVB range (14,15). Thirteen of 30 sun-sensitive LE patients reported fatigue, headache, rash, or joint pain following exposure to fluorescent light for less than 1 hour (13). Only recently has phototesting of patients with LE been performed in the UVA range as well as the UVB range (9,lO). Skin lesions clinically and histopathologically compatible with those of LE were induced by the UVB range in 33%, by the UVA range in 14%, and by both the UVA range and the UVB range in 53% of the patients tested (9). In another study, 10 of 16 patients with LE showed an abnormal response to UVA as well as UVB light (10).Herein we report a case of occupationally related exacerbation of cutaneous LE of the hands, induced by repeated exposure to UVA radiation from a photocopy machine. Phototesting of responses to UVA and UVB with serial histopathologic examinations at the irradiated sites confirmed that both wavelengths could induce this patient's disease. The UV output from 8 randomly selected photocopy machines was also determined. CASE REPORTThe patient was a 34-year-old woman with a 4-year history of SLE characterized by arthritis, photosensitivity, leukopenia, and hypocomplementemia.

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Section: Discussionmentioning

confidence: 99%

“…atous plaques, have been reproduced experimentally in individuals with LE by UVB exposure from a hot quartz or a fluorescent sunlamp (4)(5)(6)(8)(9)(10)(11). Freeman et a1 showed induction of clinically and histologically lupus-like skin lesions in 8 of 10 patients with LE following exposure to UVB at 300 nrn.…”

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confidence: 99%

Photoexacerbation of cutaneous lupus erythematosus due to ultraviolet a emissions from a photocopier

Klein

Elmets

Callen

1995

Arthritis & Rheumatism

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“…Autoantibodies may be related to the pathogenesis of cutaneous LE since deposits of immunoglobulin and complement occur at the dermal-epidermal junction in LE patients, especially in sun-exposed skin (3). These deposits can be induced experimentally by UVL (4), and are associated with the inflammatory infiltrate and with keratinocyte damage seen in cutaneous LE. It has been shown that UVL induces the release of nuclear antigens which bind with specific antibody in the skin (5), but the cellular source of these antigens and the mechanism of release has not been well-studied.…”

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confidence: 99%

Ultraviolet light induces binding of antibodies to selected nuclear antigens on cultured human keratinocytes.

LeFeber¹,

Norris²,

Ryan³

et al. 1984

J. Clin. Invest.

321

114

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Abstract. Antibodies which bind to different nuclear antigens in tissue sections or in permeabilized cell cultures are useful markers of subsets of connective tissue disease, especially of lupus erythematosus (LE), but whether these antibodies are able to react with these intracellular sequestered antigens in vivo and cause immunologic tissue damage has been a matter of much debate. We report experiments which show that ultraviolet light-irradiated, cultured human keratinocytes bind IgG antibodies from the sera of LE patients with either monospecific anti-SSA/Ro, anti-RNP, or anti-Sm activity, which implies that these antigens have been made accessible on the cell surface by ultraviolet irradiation. Normal human sera or LE patient's sera with antidouble-stranded DNA, anti-single-stranded DNA, or antihistone activity do not bind to the surface of irradiated human keratinocytes. In control experiments, all antisera produced the expected patterns of nuclear and cytoplasmic staining of fixed permeabilized, unirradiated keratinocytes. Careful study of the viability and permeability of irradiated keratinocytes by several techniques showed that this apparent cell membrane expression of extractable nuclear antigens (SSA/Ro, RNP, and Sm) following irradiation was seen on injured keratinocytes whose cell membranes were intact, but not on dead cells. It is particularly significant that all six monospecific

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“…They suggested that this could be the mechanism of photosensitive induction of disease activity and exacerbation in cases of SLE. Cripps and Rankin (1973) found the immune deposition at the dermal-epidermal junction several weeks after exposure of skin of the patients with disseminated discoid lupus erythematosus to UV light of wavelength of 250-313 nm. Davis (1977) demonstrated that antibodies to UV-DNA were detectable in sera of SLE patients but not in sera of the patients with other photodermatoses.…”

Section: Introductionmentioning

confidence: 98%

Study of DNA repair of the fibroblasts from patients with systemic lupus erythematosus

1986

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SummaryAn ability of the fibroblasts to repair ultraviolet (UV)-induced damage of DNA was investigated in patients with systemic lupus erythematosus (SLE). Unscheduled DNA synthesis (UDS) and survival rate in SLE fibroblasts were not reduced in comparison with those in normal fibroblasts, as Cleaver had reported previously (1970). In addition, sera from SLE patients had no effects on UDS. In the fibroblast colony studies, some clones exhibited decreased UDS, though mean UDS of all colonies was approximately same among different individuals. This intra-individual clonal variation in UDS occurred in both SLE patients and controls. These results indicate that the capacity of DNA repair of the fibroblasts from SLE patients is at the same level as those from normal individuals. In SLE patients, however, such cione(s) of cells with decreased level of DNA repair may present the damaged DNA induced by UV light as antigen, which will form the immune complexes under an abnormal immune responsiveness, leading to the development of photosensitivity.

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Action spectra of lupus erythematosus and experimental immunofluorescence

Cited by 51 publications

References 0 publications

Photoexacerbation of cutaneous lupus erythematosus due to ultraviolet a emissions from a photocopier

Photoexacerbation of cutaneous lupus erythematosus due to ultraviolet a emissions from a photocopier

Ultraviolet light induces binding of antibodies to selected nuclear antigens on cultured human keratinocytes.

Study of DNA repair of the fibroblasts from patients with systemic lupus erythematosus

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