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  • Key words: HSP —α-MSH — Merkel cells — UV dermatitis — Contact dermatitis  (1)
  • Schlüsselwörter Desmosomale Cadherine  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Immunohistochemical characterization of HSP, α-MSH, Merkel cells and neuronal markers in acute UV dermatitis and acute contact dermatitis in vivo (1997)
    Springer
    Inflammation research 46 (1997), S. 409-411 
    Details
    ISSN: 1420-908X
    Keywords: Key words: HSP —α-MSH — Merkel cells — UV dermatitis — Contact dermatitis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Objective: To study the immunoneurocrine network in inflammatory dermatoses, we investigated histochemically acute UV and acute contact dermatitis.¶Methods: Antibodies were applied to frozen and paraffin specimens of human skin after irradiation (n = 10), to positive patch tests (n = 10) and controls (n = 10) against: HSP 70, 72, 27, neuronal polypeptides (α-MSH, NSE, bombesin, PGP 9.5, NGF, NGF-R) and intermediate filaments (peripherin, NF 200, CK 19, 20).¶Results: HSPs and α-MSH were upregulated in UV dermatitis in the epidermis compared to contact dermatitis and normal skin. Sunburn cells did not express HSPs or α-MSH in UV dermatitis. Neuronal markers and HSP 27 labeled more nerve fibers in UV than in contact dermatitis, except the increased staining for NGF, NGF-R and α-MSH in nerve fibers in contact dermatitis. In UV dermatitis, 50% of Merkel cells were suprabasal, but in contact dermatitis, basal, rounded and reduced in number.¶Conclusions: Merkel cells, HSPs and markers of neuroinflammation are of different importance in UV and contact dermatitis in vivo.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s000110050212
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  • 2
    Electronic Resource
    Electronic Resource
    Zelluläre Adhäsionsmoleküle und Komponenten der extrazellulären Matrix als Zielstrukturen der Autoimmunität (1996)
    Springer
    Der Pathologe 17 (1996), S. 254-261 
    Details
    ISSN: 1432-1963
    Keywords: Schlüsselwörter Desmosomale Cadherine ; Hemidesmosomen ; Basalmembran ; Bullöse Dermatosen ; Goodpasture-Syndrom ; Key words Desmosomal cadherins ; Hemidesmosomes ; Basement membrane ; Blistering skin diseases ; Goodpasture's syndrome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Cell-cell and cell-matrix adhesion molecules as well as extracellular matrix components are target structures of antibody-mediated autoimmunity that have recently been well characterized at the molecular biological level. Pathogenic autoantibodies against these molecules are causally related to disturbances of cell and tissue adhesion that become apparent as various (muco-)cutaneous blistering diseases. Desmosomal cadherins (desmogleins and desmocollins) mediate epidermal intercellular adhesion. Among these, desmoglein 1 and desmoglein 3 are the autoantigens of pemphigus foliaceus and pemphigus vulgaris, respectively, exhibiting intraepidermal blistering. The pathogenic relevance of autoantibodies against desmocollins (IgA pemphigus) and desmoplakins (paraneoplastic pemphigus) still remains unclear. Hemidesmosomes contain the plaque protein BPAG1 and the partly collagen-like transmembrane protein BPAG2, representing the autoantigens of bullous pemphigoid and pemphigoid gestationis with subepidermal blistering. A certain subtype of cicatricial (benign mucous membrane) pemphigoid is characterized by autoantibodies against laminin 5 present in the subhemidesmosomal anchoring filaments, while epidermolysis bullosa acquisita and bullous SLE exhibit autoantibodies against collagen type VII constituting the anchoring fibrils. In addition, autoantibodies against a particular collagen type IV chain of the glomerular basement membrane are responsible for the manifestation of Goodpasture's syndrome. These recent molecular biological findings might be the basis for the development of novel therapeutic strategies.
    Notes: Zusammenfassung Zell-Zell- und Zell-Matrix-Adhäsionsmoleküle sowie Basalmembranbestandteile sind molekularbiologisch inzwischen sehr gut charakterisierte Zielstrukturen humoraler Autoimmunität. Pathogene Autoantikörper sind dabei kausal mit Adhäsionsstörungen v. a. im Bereich der Epidermis verbunden, die sich als verschiedenartige bullöse Dermatosen manifestieren. In Desmosomen vermitteln desmosomale Cadherine (Desmogleine und Desmocolline) die interzelluläre Adhäsion der epidermalen Keratinozyten. Von diesen sind Desmoglein 1 bzw. Desmoglein 3 die Autoantigene des Pemphigus foliaceus bzw. des Pemphigus vulgaris mit intraepidermaler Blasenbildung. Die pathogene Bedeutung von Autoantikörpern gegen Desmocolline (IgA-Pemphigus) sowie Desmoplakine (paraneoplastischer Pemphigus) ist dagegen unklar. Hemidesmosomen enthalten das Plaqueprotein BPAG1 und das kollagenartige Transmembranprotein BPAG2, die die Autoantigene für das bullöse Pemphigoid und das Pemphigoid gestationis – mit subepidermaler Blasenbildung – darstellen. Eine bestimmte Unterform des vernarbenden (Schleimhaut-)Pemphigoids ist durch Autoantikörper gegen Laminin 5 der subhemidesmosomalen Verankerungsfilamente gekennzeichnet, die Epidermolysis bullosa acquisita und der bullöse SLE durch solche gegen Kollagen VII der Verankerungsfibrillen. Ferner sind Autoantikörper gegen eine Kollagen-IV-Kette der glomerulären Basalmembran für die Manifestation des Goodpasture-Syndroms verantwortlich. Aus diesen molekularbiologischen Erkenntnissen könnten Ansatzpunkte für neue therapeutische Strategien resultieren.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002920050163
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    Paper (German National Licenses)
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