Orodigital Pemphigus Vulgaris: A Pathogenic Role of Anti-Desmoglein-3 Autoantibodies in Pemphigus Paronychia?

Dermatology ◽  
2008 ◽  
Vol 217 (4) ◽  
pp. 337-339 ◽  
Author(s):  
Emmanuel Laffitte ◽  
Renato G. Panizzon ◽  
Luca Borradori
2021 ◽  
Vol 141 (10) ◽  
pp. S154
Author(s):  
A. Zakrzewicz ◽  
C. Würth ◽  
B. Beckert ◽  
S. Feldhoff ◽  
P. Verheesen ◽  
...  

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Rodolfo Pessato Timoteo ◽  
Marcos Vinicius da Silva ◽  
Camila Botelho Miguel ◽  
Djalma Alexandre Alves Silva ◽  
Jonatas Da Silva Catarino ◽  
...  

Pemphigus vulgaris (PV) is an autoimmune disease characterized by the presence of IgG autoantibodies against desmoglein-3. Despite the variety of findings, the chemokine and cytokine profiles that characterize the immune response in the disease are still poorly explored. Thus, 20 PV patients and 20 controls were grouped according to gender, ethnicity, place of residence, and clinical parameters of the disease. Then, the levels of chemokines and of Th1/Th2/Th17/Treg/Th9/Th22-related cytokines were assessed in the serum. PV patients had higher levels of inflammatory Th1/Th17 cytokines (IFN-γ, IL-17, and IL-23), as well as higher levels of CXCL8 and reduced levels of Th1/Th2-related chemokines (IP-10 and CCL11). However, no differences in the levels of IL-2, IL-6, TNF-α, IL-1β, IL-4, IL-9, IL-12, TGF-β, IL-33, MCP-1, RANTES, and MIP-1α were found between PV patients and their control counterparts. Furthermore, PV patients with skin lesions had higher serum levels of IL-6 and CXCL8 when compared to PV patients without lesions. Taken together, our findings describe the role of cytokines and chemokines associated with Th1/Th17 immune response in PV patients. Finally, these data are important for better understanding of the immune aspects that control disease outcome, and they may also provide important information about why patients develop autoantibodies against desmogleins.


Life ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 621
Author(s):  
Ambreen Rehman ◽  
Yunying Huang ◽  
Hong Wan

The immunobullous condition Pemphigus Vulgaris (PV) is caused by autoantibodies targeting the adhesion proteins of desmosomes, leading to blistering in the skin and mucosal membrane. There is still no cure to the disease apart from the use of corticosteroids and immunosuppressive agents. Despite numerous investigations, the pathological mechanisms of PV are still incompletely understood, though the etiology is thought to be multifactorial. Thus, further understanding of the molecular basis underlying this disease process is vital to develop targeted therapies. Ample studies have highlighted the role of Desmoglein-3 (DSG3) in the initiation of disease as DSG3 serves as a primary target of PV autoantibodies. DSG3 is a pivotal player in mediating outside-in signaling involved in cell junction remodeling, cell proliferation, differentiation, migration or apoptosis, thus validating its biological function in tissue integrity and homeostasis beyond desmosome adhesion. Recent studies have uncovered new activities of DSG3 in regulating p53 and the yes-associated protein (YAP), with the evidence of dysregulation of these pathways demonstrated in PV. The purpose of this review is to summarize the earlier and recent advances highlighting our recent findings related to PV pathogenesis that may pave the way for future research to develop novel specific therapies in curing this disease.


2017 ◽  
pp. 66-71
Author(s):  
O. Yablon ◽  
◽  
N. Zaichko ◽  
O. Mazulov ◽  
Z.I. Rossokha ◽  
...  

10.2741/2875 ◽  
2008 ◽  
Vol 13 (13) ◽  
pp. 2686 ◽  
Author(s):  
Toshiyuki Yamamoto
Keyword(s):  

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