Naslov
Desmoglein Story from Masayuki Amagai Teach us How to Discover the Beauty of Nature

Autori
Lipozenčić, Jasna ; Marinović, Branka

Izvornik
Acta dermatovenerologica Croatica (1330-027X) 15 (2007), 4; 274-275

Vrsta, podvrsta i kategorija rada
Radovi u časopisima, vijest, stručni

Ključne riječi
desmoglein ; molecular structure ; oral presentation

Sažetak
It was wonderful after so many years of learning about epidemiology nature, diagnostic and management of pemphigus group and other bullous dermatoses in University Department of Dermatology and Venereology Zagreb University Hospital Center and School of Medicine to discover out of oral presentation of Prof. Michael Hertl “ Bullöse Dermatosen 2007” in Graz (Austria) on 3. Derm Akademie Graz, on October 20, 2007 the beauty of the exact molecular mechanism of the pathogenesis of pemphigus and cell-cell adhesion of keratinocytes that solved us the question of desmoglein as transmembrane glycoprotein of the desmosome. The modern history of pemphigus began with the discovery of circulating antibodies against the cell surface of keratinocytes in the sera of patients with pemphigus vulgaris (PV) by Beutner and Jordan in 1964. In the late 1970s and early 1980s, it was demonstrated that autoantibodies in pemphigus are pathogenic and induce blister formation in skin organ culture systems and Anhalt demonstrated IgG passive transfer of patients to neonatal mice. Stanley et al in 1982 identified PV antigen in PV sera as glycosylated 130-¬ ; kDa glycoprotein, later showed Hashimoto epidermal extracts binding to 130-kDa polypeptide and in 1984 Stanley et al first characterized pemphigus foliaceus (PF) antigen as a polypeptide of about 160-kDa and recognized by PF sera as identical to desmoglein 1 (Dsg). In 1991 Amagai et al iso¬ ; lated a cDNA clone for the PV antigen from the sera of patients with PV. Both Dsg1 and PV antigen are cadherin-type adhesion molecules that occur in desmosomes. PV antigen is termed desmoglein 3 (Dsg3) closely related to Dsg1.IgG autoantibodies against Dsg1 and Dsg3 are pathogenic and induce blister formation in pemphigus and can cause suprabasilar acantholysis, the typical histologic finding in PV. Thus, pemphigus has been redefined as an antidesmoglein autoimmune disease. PV can be divided into 2 subgroups: the mucosal dominant type (anti Dsg3 IgG) with minimal blister skin involvement, and the mucocutaneous type, with extensive skin blisters and mucosal involvement with anti¬ ; Dsg3 and anti-Dsg1 IgG with distinct intraepithelial expression patterns. Patients with PF have only anti-Dsg1 IgG autoantibodies which are insufficient to induce blisters in neonatal skin which is rare absent in pregnant woman with pemphigus but in neonates of mothers with PV have blisters develop. PF share with staphylococcal scaled skin syndrome (SSSS) many similar features: both disease involve only the skin, have desmoglein 1 autoantibodies and shows superficial epidermal separation. It is Now we known that PV and PF had different autoantigens. We dermatologists see many different skin lesions that consist of a variety of different shapes. The meaning as to why it is formed in that way we could enjoyed in lecture of Prof. Hertl in Graz. As Prof. Masayuki Amagai said, “ the nature shows amazing beauty and logic. If you continue seeing the shape of skin lesions with your own eyes in your daily practice, you will have plenty of chances to discover the beauty of nature” .

Izvorni jezik
Engleski

Znanstvena područja
Kliničke medicinske znanosti

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