Immunohistochemistry of Ultraviolet-Induced Pemphigus and Pemphigoid Lesions

Cram, David L.

doi:10.1001/archderm.1972.01620150005001

Cited by 113 publications

(32 citation statements)

References 15 publications

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“…The clinical, histological and immuno logical findings were consistent with pemphigus vulgaris. After a heavy sun exposure, however, a severe exacerbation occurred, consistent with several reports [3,4], In addition to the intercellular deposits of Ig and C in the Malpighian layer consistent with pemphigus vulgaris, concomitant granular deposits of IgG and C3 were demonstrated at the dermal epidermal junction, similar to the findings in LE. The lack of antinuclear antibodies and the negative LE cell phenomenon may be explained by the data reported by Fessel [5], that a subgroup of LE, about 5% of the cases, have repeatedly negative tests for antinuclear antibodies and the LE cell phenomenon.…”

Section: Discussionsupporting

confidence: 90%

Basement Membrane Zone Deposits of Immunoglobulins and Complement in a Patient with Pemphigus vulgaris

Livden

1980

Dermatology

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Section: Discussionsupporting

confidence: 90%

Basement Membrane Zone Deposits of Immunoglobulins and Complement in a Patient with Pemphigus vulgaris

Livden

1980

Dermatology

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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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“…2). Most cases occur sporadically although ultraviolet light and several medications have found to be potential triggers [37].…”

Section: Bullous Pemphigoidmentioning

confidence: 99%

Skin Manifestations of Internal Disease in Older Adults

Markus¹,

Perry²,

Lear³

2015

Curr Geri Rep

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The skin is the largest and most visible organ in the body and can give diagnostic clues of systemic illness. These clues often become obscured through the normal aging process. The purpose of this review is to give an overview of the normal skin changes seen with aging and then discuss new findings with regards to cutaneous signs of systemic disease in the elderly. We performed a literature search on cutaneous manifestations of internal disease and limited our search to articles published within the last 5 years. We then narrowed down the articles on conditions that primarily affect the adults over the age of 65; conditions commonly seen in the elderly as well as new findings which we felt were of great significance. Ultimately, we hope to update the reader on new cutaneous diagnostic tools of internal disease.

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Immunohistochemistry of Ultraviolet-Induced Pemphigus and Pemphigoid Lesions

Cited by 113 publications

References 15 publications

Basement Membrane Zone Deposits of Immunoglobulins and Complement in a Patient with Pemphigus vulgaris

Basement Membrane Zone Deposits of Immunoglobulins and Complement in a Patient with Pemphigus vulgaris

Effects of UVB on the Synthesis of Complement Proteins by Keratinocytes

Skin Manifestations of Internal Disease in Older Adults

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