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Commonality of the IL-4/IL-13 pathway in atopic diseases
被引:356
|作者:
Gandhi, Namita A.
[1
]
Pirozzi, Gianluca
[2
]
Graham, Neil M. H.
[3
]
机构:
[1] Regeneron Pharmaceut Inc, Clin Sci, 777 Old Saw Mill River Rd, Tarrytown, NY 10591 USA
[2] Sanofi, Res & Dev, Bridgewater, NJ USA
[3] Regeneron Pharmaceut Inc, Project Direct, 777 Old Saw Mill River Rd, Tarrytown, NY 10591 USA
关键词:
interleukin-4;
interleukin-13;
dupilumab;
lebrikizumab;
tralokinumab;
Type;
2;
pathway;
asthma;
atopic dermatitis;
nasal polyposis;
ACTIVATION-REGULATED CHEMOKINE;
DOUBLE-BLIND;
PERSISTENT ASTHMA;
ADULT PATIENTS;
SERUM THYMUS;
INTERLEUKIN-4;
RECEPTOR;
ORAL CYCLOSPORINE;
ALLERGIC DISEASES;
STRUCTURAL BASIS;
CLUSTER-ANALYSIS;
D O I:
10.1080/1744666X.2017.1298443
中图分类号:
R392 [医学免疫学];
Q939.91 [免疫学];
学科分类号:
100102 ;
摘要:
Introduction: Allergy results from an aberrant Type 2 inflammatory response, triggered by a wide range of environmental antigens (allergens) that lead to various immune responses, culminating in the production of immunoglobulin E (IgE). Two key cytokines, interleukin (IL)-4 and IL-13, are critical to the induction and perpetuation of the Type 2 response, and have been implicated in multiple atopic diseases.Area covered: This review summarizes recent milestone developments that have elucidated components of the pathogenesis of atopic diseases such as atopic dermatitis (AD), asthma, and chronic sinusitis with nasal polyposis (CSwNP).Expert commentary: Several therapeutic agents that selectively target potentiators of the Type 2 pathway have shown efficacy in one or more of these atopic diseases, but few agents have proven to be broadly applicable across all three atopic diseases. Dupilumab, a human monoclonal antibody that simultaneously inhibits signaling of IL-4 and IL-13, has demonstrated significant clinical efficacy in AD, asthma, and CSwNP. The fact that these diseases often occur as comorbidities and respond to the same therapy suggests that there is a common underlying pathogenic pathway, and that IL-4 and IL-13 cytokines are central to regulating the pathogenesis of these atopic diseases.
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页码:425 / 437
页数:13
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