Interleukin 4 inhibition as a potential therapeutic in pemphigus

被引:49
作者
Tavakolpour, Soheil [1 ]
Tavakolpour, Vahid [2 ]
机构
[1] Razi Hosp, Dept Dermatol, Bullous Dis Res Ctr, Tehran, Iran
[2] Stem Cell Technol Res Ctr, Tehran, Iran
关键词
Interleukin-4; Pemphigus; Anti-cytokine therapy; Autoimmune disease; REGULATORY T-CELLS; INTERFERON-GAMMA; DIFFERENTIAL REGULATION; RITUXIMAB THERAPY; ANTIDESMOGLEIN; DISEASE-ACTIVITY; GENE-EXPRESSION; IGG4; PRODUCTION; IGE SYNTHESIS; SERUM-LEVELS;
D O I
10.1016/j.cyto.2015.09.017
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Pemphigus is an autoimmune bullous skin disease that results from desmosomal protein desmoglein 3 and 1 loss in pemphigus vulgaris and foliaceus, respectively. It can be considered as a Th2-dominant disease over-expressed by Th2 cell cytokines. Interleukin (IL)-4 is a key cytokine which can exacerbate Th2 over-expression in addition to isotype switching to immunoglobin (Ig)G1 and IgG4 that are responsible for desmoglein loss. Elevation of IL-4 level has also been reported in various studies. Considering the important role of IL-4 in severe phase of pemphigus and lack of effective and safeness therapy for this potentially fatal disease, anti-IL-4 therapy was introduced as a potential curative for pemphigus disease. This study reviewed all studies about any roles of IL-4 that can directly and indirectly be played in the development of pemphigus and IL-4 inhibition with interferons and dupilumab therapy were introduced as a novel pemphigus treatment for patients who are in relapse phase of the disease. Dupilumab was also introduced as a possible treatment for patients with severe pemphigus. It can directly inhibit IL-4 by targeting IL-4 alpha-chain receptor. IL-4 inhibition can lead to the creation of Th1 :Th2 balance by various pathways, discussed in this study. (C) 2015 Elsevier Ltd. All rights reserved.
引用
收藏
页码:189 / 195
页数:7
相关论文
共 103 条
[1]   Pemphigus in South Africa [J].
Aboobaker, J ;
Morar, N ;
Ramdial, PK ;
Hammond, MG .
INTERNATIONAL JOURNAL OF DERMATOLOGY, 2001, 40 (02) :115-119
[2]  
Afshari JT, 2007, IRAN J ALLERGY ASTHM, V6, P67
[3]   Treatment of pemphigus vulgaris with rituximab and intravenous immune globulin [J].
Ahmed, A. Razzaque ;
Spigelman, Zachary ;
Cavacini, Lisa A. ;
Posner, Marshall R. .
NEW ENGLAND JOURNAL OF MEDICINE, 2006, 355 (17) :1772-1779
[4]   Immunogenicity of Anti-TNF-α Agents in Autoimmune Diseases [J].
Aikawa, Nadia Emi ;
de Carvalho, Jozelio Freire ;
Almeida Silva, Clovis Artur ;
Bonfa, Eloisa .
CLINICAL REVIEWS IN ALLERGY & IMMUNOLOGY, 2010, 38 (2-3) :82-89
[5]   Role of interleukin 10 in specific immunotherapy [J].
Akdis, CA ;
Blesken, T ;
Akdis, M ;
Wüthrich, B ;
Blaser, K .
JOURNAL OF CLINICAL INVESTIGATION, 1998, 102 (01) :98-106
[6]   Interleukins, from 1 to 37, and interferon-γ: Receptors, functions, and roles in diseases [J].
Akdis, Muebeccel ;
Burgler, Simone ;
Crameri, Reto ;
Eiwegger, Thomas ;
Fujita, Hiroyuki ;
Gomez, Enrique ;
Klunker, Sven ;
Meyer, Norbert ;
O'Mahony, Liam ;
Palomares, Oscar ;
Rhyner, Claudio ;
Quaked, Nadia ;
Schaffartzik, Anna ;
Van De Veen, Willem ;
Zeller, Sabine ;
Zimmermann, Maya ;
Akdis, Cezmi A. .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2011, 127 (03) :701-U317
[7]  
Alter M, 2009, HAUTARZT, V60, P743, DOI 10.1007/s00105-008-1682-0
[8]   AUTOANTIBODIES AGAINST A NOVEL EPITHELIAL CADHERIN IN PEMPHIGUS-VULGARIS, A DISEASE OF CELL-ADHESION [J].
AMAGAI, M ;
KLAUSKOVTUN, V ;
STANLEY, JR .
CELL, 1991, 67 (05) :869-877
[9]   The clinical phenotype of pemphigus is defined by the anti-desmoglein autoantibody profile [J].
Amagai, M ;
Tsunoda, K ;
Zillikens, D ;
Nagai, T ;
Nishikawa, T .
JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY, 1999, 40 (02) :167-170
[10]   Modern Anti-Cytokine Therapy of Autoimmune Diseases [J].
Astrakhantseva, I. V. ;
Efimov, G. A. ;
Drutskaya, M. S. ;
Kruglov, A. A. ;
Nedospasov, S. A. .
BIOCHEMISTRY-MOSCOW, 2014, 79 (12) :1308-1321