J. Elsner et A. Kapp, Modulation of eosinophil effector functions: The potential role of monoclonal antibodies and chemokine receptor antagonists, ALL ASTH P, 21(6), 2000, pp. 345-349
Increased numbers of eosinophils in the peripheral blood and inflammatory t
issue are characteristic features of allergic diseases such as allergic ast
hma, rhinoconjunctivitis, and atopic dermatitis. Tissue damage and propagat
ion of inflammation is thought to be mediated by the interaction among Th2-
like T cells, antigen-presenting cells, and eosinophils. In this process eo
sinophils are activated by several inflammatory mediators, leading to the i
nflux of eosinophils at sires of inflammation and to tissue damage by the r
elease of reactive oxygen species and toxic granule proteins. Therefore, ag
ents that would be able to inhibit or antagonize mediator-induced eosinophi
l activation seem to be possibilities as new therapeutic strategies. In thi
s review we will focus on the modulation of human eosinophil effector funct
ions by monoclonal antibodies and chemokine receptor antagonists. We will d
iscuss whether modulation of eosinophil effector functions might be success
ful as a possible future strategy of diseases that are accompanied by activ
ated eosinophils. Even when these compounds shaw antagonistic effects on hu
man eosinophils, in vitro future studies will be necessary to investigate w
hether chemokine receptor antagonists and monoclonal antibodies are suitabl
e in vivo in an animal model prior to studies in humans.