Induction of antinuclear antibodies by ultraviolet irradiation.

Veen, J; Lucas, C.J.

doi:10.1136/ard.29.5.556

Cited by 13 publications

(2 citation statements)

References 6 publications

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“…Views on photoreactivation phenomena in mam malian cells are divergent. Our results do not confirm those of Ten Veen (13), who observed an influence of daylight on UV-DNA repair. In our experiments, the lF reaction became negative at the same lime in mice kept in darkness and those exposed to day light.…”

Section: Immunological Phenomena Induced By V V Rays 17contrasting

confidence: 99%

Immunological phenomena induced by UV rays

Jarzabek-Chorzelska¹,

Zarebska²,

Wolska³

et al. 1976

Acta Derm Venereol

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Antiserum against UV-irradiated DNA was prepared and used as a specific reagent in an indirect immunofluorescence (IF) technique for the detection of photochemically damaged DNA in the epidermis of hairless mice. Fluorescence of cell nuclei was found in sections of dorsal epidermis of mice immediately after the irradiation. It persisted for 24 hours. The IF reaction became negative after 48 hours, irrespective of the duration of UV exposure to which the mice were subjected. This may indicate: either (a) the occurrence of DNA repair processes, or (b) the relation of DNA repair to the life cycle of the epidermal cell. Mice exposed to UV radiation similar to the erythema spectrum of sunlight do not show any changes in the cellular DNA, even after a dose of 40 MED.

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Section: Immunological Phenomena Induced By V V Rays 17contrasting

confidence: 99%

Immunological phenomena induced by UV rays

Jarzabek-Chorzelska¹,

Zarebska²,

Wolska³

et al. 1976

Acta Derm Venereol

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“…Therefore, although our chronic UVR exposure model represented a convenient in vivo experimental system in which the effect of C1q de®ciency on continual apoptotic keratinocyte production could be studied, it also created a milieu that favored immunologic nonresponsiveness. Although an early study did report the development of ANA in female Swiss mice exposed to UVR, the UV source was predominantly in the UVC spectral range and the majority of ANA detected were of low titer (`1 in 80) (Veen and Lucas, 1970).…”

Section: Discussionmentioning

confidence: 99%

Ultraviolet-Radiation-Induced Keratinocyte Apoptosis in C1q-Deficient Mice

Pickering

Fischer

Lewis

et al. 2001

Journal of Investigative Dermatology

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Exposure to ultraviolet B radiation is an important trigger of both systemic and cutaneous disease flares in individuals with systemic lupus erythematosus. More than 90% of individuals with homozygous C1q deficiency develop a systemic-lupus-erythematosus-like illness, which is typically associated with a severe photosensitive rash. Apoptotic, human keratinocytes have been shown in vitro to bind C1q, in the absence of antibody. These observations, together with the hypothesis that a major source of the autoantigens driving the immune response in systemic lupus erythematosus comes from apoptotic cells, led us to investigate the effects of murine C1q deficiency on ultraviolet-radiation-induced keratinocyte apoptosis in vivo. In this work, we demonstrated C1q binding to apoptotic murine keratinocytes in vitro and showed for the first time that C1q is also present on sunburn cells in vivo. In addition to C1q, we detected C3 deposition on sunburn cells in both wild-type and C1q-deficient mice, suggesting activation of the alternative pathway. Following acute ultraviolet exposure in vivo, no difference in the rate of clearance of sunburn cells was found in C1q-deficient mice from three different genetic backgrounds, compared with strain-matched wild-type controls. Furthermore, chronic ultraviolet exposure did not result in the production of autoantibodies or the development of glomerulonephritis. Our findings suggest that C1q does not play a critical role in the physiologic clearance of apoptotic murine keratinocytes in vivo.

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Systemic lupus erythematosus: association with psoralen--ultraviolet-A treatment of psoriasis

Eyanson¹

1979

Archives of Dermatology

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Systemic lupus erythematosus (SLE) developed in as 23-year-old woman with psoriasis during treatment with psoralen-ultraviolet-A (PUVA). The connective tissue disease was characterized by an erythematous rash, hair loss, nephritis, splenomegaly, seizures, and coma. Serum antinuclear antibodies were present in high titer, and hypocomplementemia developed. Antibodies to native or ultraviolet-irradiated DNA were not demonstrated. While the association of psoriasis and lupus may have been fortuitous, the temporal relationships suggest that PUVA treatment in this case may have been of pathogenetic importance in the development of the connective tissue disease.

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Induction of antinuclear antibodies by ultraviolet irradiation.

Cited by 13 publications

References 6 publications

Immunological phenomena induced by UV rays

Immunological phenomena induced by UV rays

Ultraviolet-Radiation-Induced Keratinocyte Apoptosis in C1q-Deficient Mice

Systemic lupus erythematosus: association with psoralen--ultraviolet-A treatment of psoriasis

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