An Overview of the Safety and Efficacy of Monoclonal Antibodies for the Chronic Obstructive Pulmonary Disease
Mario Cazzola,1 Josuel Ora,2 Francesco Cavalli,1 Paola Rogliani,1,2 Maria Gabriella Matera3 1Chair of Respiratory Medicine, Department of Experimental Medicine, University of Rome Tor Vergata, Rome, Italy; 2Division of Respiratory Medicine, University Hospital Tor Vergata, Rome, Italy; 3Chair of Pha...
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| Formato: | article |
| Lenguaje: | EN |
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Dove Medical Press
2021
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| Acceso en línea: | https://doaj.org/article/b877eba557124db2b2b32274aeae2752 |
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| Sumario: | Mario Cazzola,1 Josuel Ora,2 Francesco Cavalli,1 Paola Rogliani,1,2 Maria Gabriella Matera3 1Chair of Respiratory Medicine, Department of Experimental Medicine, University of Rome Tor Vergata, Rome, Italy; 2Division of Respiratory Medicine, University Hospital Tor Vergata, Rome, Italy; 3Chair of Pharmacology, Department of Experimental Medicine, University of Campania Luigi Vanvitelli, Naples, ItalyCorrespondence: Mario Cazzola Email mario.cazzola@uniroma2.itAbstract: Several mAbs have been tested or are currently under clinical evaluation for the treatment of COPD. They can be subdivided into those that aim to block specific pro-inflammatory and pro-neutrophilic cytokines and chemokines, such as TNF-α, IL-1β, CXCL8 and IL-1β, and those that act on T2-mediated inflammation, respectively, by blocking IL-5 and/or its receptor, preventing IL-4 and IL-13 signaling, affecting IL-33 pathway and blocking TSLP. None of these approaches has proved to be effective, probably because in COPD there is no dominant cytokine or chemokine and, therefore, a single mAb cannot be effective on all pathways. With a more in-depth understanding of the numerous pheno/endotypic pathways that play a role in COPD, it may eventually be possible to identify those specific patients in whom some of these cytokines or chemokines might predominate. In this case, it will be possible to implement a personalized treatment, but the use of each mAb will only be reserved for a very limited number of subjects.Keywords: COPD, monoclonal antibodies, pheno/endotypic pathways, anti–T1-mediated inflammation mAbs, anti–T2-mediated inflammation mAbs |
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