TY - JOUR
T1 - Emerging Functions of Amphiregulin in Orchestrating Immunity, Inflammation, and Tissue Repair
AU - Zaiss, Dietmar
AU - Gause, William C.
AU - Osborne, Lisa C
AU - Artis, David
N1 - Date of Acceptance:17/02/2015
MR/M011755/1
PY - 2015/1/1
Y1 - 2015/1/1
N2 - Type 2 inflammatory responses can be elicited by diverse stimuli, including toxins, venoms, allergens, and infectious agents, and play critical roles in resistance and tolerance associated with infection, wound healing, tissue repair, and tumor development. Emerging data suggest that in addition to characteristic type 2-associated cytokines, the epidermal growth factor (EGF)-like molecule Amphiregulin (AREG) might be a critical component of type 2-mediated resistance and tolerance. Notably, numerous studies demonstrate that in addition to the established role of epithelial- and mesenchymal-derived AREG, multiple leukocyte populations including mast cells, basophils, group 2 innate lymphoid cells (ILC2s), and a subset of tissue-resident regulatory CD4+ T cells can express AREG. In this review, we discuss recent advances in our understanding of the AREG-EGF receptor pathway and its involvement in infection and inflammation and propose a model for the function of this pathway in the context of resistance and tissue tolerance.
AB - Type 2 inflammatory responses can be elicited by diverse stimuli, including toxins, venoms, allergens, and infectious agents, and play critical roles in resistance and tolerance associated with infection, wound healing, tissue repair, and tumor development. Emerging data suggest that in addition to characteristic type 2-associated cytokines, the epidermal growth factor (EGF)-like molecule Amphiregulin (AREG) might be a critical component of type 2-mediated resistance and tolerance. Notably, numerous studies demonstrate that in addition to the established role of epithelial- and mesenchymal-derived AREG, multiple leukocyte populations including mast cells, basophils, group 2 innate lymphoid cells (ILC2s), and a subset of tissue-resident regulatory CD4+ T cells can express AREG. In this review, we discuss recent advances in our understanding of the AREG-EGF receptor pathway and its involvement in infection and inflammation and propose a model for the function of this pathway in the context of resistance and tissue tolerance.
UR - http://www.scopus.com/inward/record.url?scp=84923015891&partnerID=8YFLogxK
U2 - 10.1016/j.immuni.2015.01.020
DO - 10.1016/j.immuni.2015.01.020
M3 - Article
C2 - 25692699
AN - SCOPUS:84923015891
SN - 1074-7613
VL - 42
SP - 216
EP - 226
JO - Immunity
JF - Immunity
IS - 2
ER -