Cellular and molecular regulation of eosinophil trafficking to the lung.
Airway inflammation is central to the pathogenesis of allergic asthma, and molecules that mediate this process obviously represent targets for therapy. In the present article, we discuss our experiments, which point to CD4+ T cells and IL-5-driven eosinophilia as potential targets for the relief of bronchial hyperreactivity in late-phase asthma.
Hogan
S P
SP
Division of Biochemistry, John Curtin School of Medical Research, Australian National University, Acton, Australian Capital Territory.
Mould
A W
AW
Young
J M
JM
Rothenberg
M E
ME
Ramsay
A J
AJ
Matthaei
K
K
Young
I G
IG
Foster
P S
PS
D000818:Animals; D001249:Asthma / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000502:physiology; D002465:Cell Movement / Q000502:physiology*; D054413:Chemokine CCL11; D019742:Chemokines, CC; D016207:Cytokines / Q000502:physiology; D004195:Disease Models, Animal; D004804:Eosinophils / Q000502:physiology*; D007111:Immunity, Cellular; D015847:Interleukin-4 / Q000502:physiology*; D015848:Interleukin-5 / Q000502:physiology*; D008168:Lung / Q000276:immunology; D051379:Mice; D011657:Pulmonary Eosinophilia / Q000276:immunology
C515457:Ccl11 protein, mouse; D054413:Chemokine CCL11; D019742:Chemokines, CC; D016207:Cytokines; D015848:Interleukin-5; D015847:Interleukin-4