Autoimmune Disease

Morison, Warwick L.

doi:10.1007/978-1-4613-3670-9_13

Cited by 3 publications

(2 citation statements)

References 24 publications

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“…In some autoimmune diseases, such as pemphigus, pemphigoid, discoid lupus erythematosus, and photosensitive lupus erythematosus, C deposits on keratinocytes are seen in lesional skin but can also be induced in nonlesional skin by UVB exposure (Cram and Fukuyama, 1972;Morison, 1983). In some diseases of unknown Figure 5.…”

Section: Discussionmentioning

confidence: 99%

Effects of UVB on the Synthesis of Complement Proteins by Keratinocytes

Pasch

Okada

Bos³

et al. 1998

Journal of Investigative Dermatology

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UVB exposure of the skin results in increased production of several cytokines by keratinocytes and infiltration of inflammatory cells. We hypothesized that UVB may increase the expression of complement (C) components and C-regulatory proteins by keratinocytes. In vivo, UVB may upregulate these proteins by direct effects or via cytokines released by keratinocytes or infiltrating inflammatory cells. In vitro, UVB may upregulate these proteins only directly, because of dilution of released cytokines in the medium. To test this, we exposed cultured human keratinocytes to UVB (0-64 J per m2) and monitored C3 and Factor B release in the medium by enzyme-linked immunosorbent assay, and surface expression of decay accelerating factor, membrane cofactor protein, and CD59 by flow cytometry. Keratinocytes produced small amounts of C3 and Factor B, which remained unaffected by UVB. UVB (32 J per m2) caused a transient upregulation of all three C-regulatory proteins. Decay accelerating factor expression was maximal at 48 h (1.81 +/- 0.06-fold increase in mean fluorescence intensity over nonexposed cells), membrane cofactor protein at 72 h (2.13 +/- 0.09-fold increase in mean fluorescence intensity), and CD59 at 120 h (1.96 +/- 0.09-fold increase in mean fluorescence intensity), returning to baseline values within 96, 192, and 192 h, respectively. Exposure to 64 J per m2 resulted in significant cell death; cells surviving this dose up to 48 h expressed a higher level of all the three proteins than those surviving 32 J per m2. In conclusion, UVB upregulated membrane cofactor protein, decay accelerating factor, and CD59 on keratinocytes without affecting the constitutive release of C3 and Factor B. Thus, UVB can increase the resistance of keratinocytes against their own C known to be produced excessively in response to cytokines of inflammatory cells that infiltrate the skin following UVB exposure.

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Section: Discussionmentioning

confidence: 99%

Effects of UVB on the Synthesis of Complement Proteins by Keratinocytes

Pasch

Okada

Bos³

et al. 1998

Journal of Investigative Dermatology

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“…It is known that UV irradiation enhance the lupus dermatoses in human SLE (18). A similar effect of UV has been demonstrated in nude mice (22), Swiss mice (2), and normal rabbits (15), although an Fl hybrid of New Zealand black and white mice failed to show any acceleration of autoimmune traits after UV irradiation (5).…”

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confidence: 71%

The Uterus Lupus Band Test and Its Correlation with the Skin Lupus Band Test in Autoimmune Mice

Furukawa

Horiguchi

Kanauchi

et al. 1986

Microbiology and Immunology

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Systemic lupus erythematosus (SLE) is a multisystem disease, involving the kidney, skin, spleen, and other organs. In 1963, Burnham et al (4) described a band of localized immunoglobulin (Ig) deposition at the dermo-epidermal junction (DEJ) of the skin lesion in patients with SLE. The term lupus band (LB) was used to this skin lesion (20), and the LB test (LBT) is now regarded to be of diagnostic and prognostic value in SLE. However, the immunological mechanisms of Ig deposition at the DEJ are still obscure.Several strains of SLE-prone mice have been developed for studies on the pathogenesis of SLE (13,16,19,21). Recently we found that positivity of the LBT in nonlesional skin is a common feature in New Zealand, MRL/Mp-lpr/lpr (MRL/l) and BXSB mice (7,8,11). Furthermore, this LBT positivity in New Zealand mice is regulated by genetic factors (9).Recently we observed Ig deposition along the subepithelial junction of the uterine cervix (tentatively designated uterus LB) in female MRL/1 and BXSB mice. In this study, we report the age related incidence of a positive uterus-LBT and its correlation with a positive skin-LBT and the effects of ultraviolet (UV) irradiation on the skin-LBT and uterus-LBT.MRL/1, MRL/Mp-+/ + (MRL/n), and BXSB mice were purchased from Jackson Laboratories, Bar Harbor, ME, U.S.A. BALB/c mice were obtained from our colony. These mice were maintained under specific-pathogen-free conditions. All mice used in this study were virgin females.Specimens of the uterus were obtained from the caudal portion of the uterus which was considered to be equivalent to the human uterine cervix, and those of the skin from the backs of MRL mice and the tails of BXSB and BALB/c mice. All specimens were frozen immediately in a bath of acetone and dry ice, and stored at -80 C until use.The following antisera were used: FITC-labeled anti-mouse Ig, FITC-labeled anti-mouse IgG, goat anti-mouse IgM (Cappel Laboratories, Cochranville, PA, U.S.A.), FITC-labeled anti-goat Ig (prepared in our laboratory), FITC-labeled anti-mouse C3 (Cappel), and anti-Rauscher gp 70, which was kindly donated by 395

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Seasons of the Year and Activity of SLE and Behçet's Disease

Krause

Shraga

Molad

et al. 1997

Scandinavian Journal of Rheumatology

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Patients with systemic lupus erythematosus (SLE) were evaluated using a telephone questionnaire on the activity of various disease manifestations during the seasons of the past year. The results were compared to those of patients with Behcet's disease (BD), using the same questionnaires, and analyzed in relation to the mean temperature, humidity, barometric pressure, and ultraviolet radiation (UVR) in the patient's location, obtained from the official Israeli Meteorological Service. It was found that SLE patients had a tendency towards winter worsening of clinical manifestations, shown as increased incidence of joint pains, weakness, fatigue, Raynaud's phenomenon, and rash, as well as increased number of hospital admissions, sick leaves, and need to raise the dose of medications. The symptoms of patients with BD were not correlated to seasons of the year, except for increased joint pains in autumn and spring. We suggest that UVR accumulation might cause exacerbations in SLE patients several months after prolonged exposure to sunlight in the summer.

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Autoimmune Disease

Cited by 3 publications

References 24 publications

Effects of UVB on the Synthesis of Complement Proteins by Keratinocytes

Effects of UVB on the Synthesis of Complement Proteins by Keratinocytes

The Uterus Lupus Band Test and Its Correlation with the Skin Lupus Band Test in Autoimmune Mice

Seasons of the Year and Activity of SLE and Behçet's Disease

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