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.