TY - JOUR
T1 - Role of paired Ig-like receptor-B in the humoral immune response
AU - Takai, Toshiyuki
N1 - Funding Information:
The author’s work cited in the present review is supported by the CREST Program of Japan Science and Technology Agency (JST), the Virtual Research Institute of Aging founded by Nippon Boehringer Ingelheim and by research grants from the Ministry of Education, Science, Sports and Culture of Japan.
PY - 2004/6
Y1 - 2004/6
N2 - The Ig-like receptors provide positive and negative regulation of immune cells upon recognition of various ligands, thus enabling those cells to respond adequately to extrinsic stimuli. Murine paired Ig-like receptor (PIR)-A and PIR-B, a typical receptor pair of the Ig-like receptor family, are expressed on a wide range of cells in the immune system, such as B cells, mast cells, macrophages and dendritic cells, mostly in a pair-wise fashion. The PIR-A requires the homodimeric Fc receptor common γ chain for its efficient cell-surface expression and for the delivery of activation signaling. In contrast, PIR-B inhibits receptor-mediated activation signaling in vitro upon engagement with other activating-type receptors, such as the antigen receptor on B cells and the high-affinity Fc receptor for IgE on mast cells. Although the ligands for PIR-A and PIR-B remain unknown, recent studies on PIR-B-deficient mice have provided us with valuable insight into the physiological significance of PIR-B, particularly in its regulatory role in balancing the humoral immune response.
AB - The Ig-like receptors provide positive and negative regulation of immune cells upon recognition of various ligands, thus enabling those cells to respond adequately to extrinsic stimuli. Murine paired Ig-like receptor (PIR)-A and PIR-B, a typical receptor pair of the Ig-like receptor family, are expressed on a wide range of cells in the immune system, such as B cells, mast cells, macrophages and dendritic cells, mostly in a pair-wise fashion. The PIR-A requires the homodimeric Fc receptor common γ chain for its efficient cell-surface expression and for the delivery of activation signaling. In contrast, PIR-B inhibits receptor-mediated activation signaling in vitro upon engagement with other activating-type receptors, such as the antigen receptor on B cells and the high-affinity Fc receptor for IgE on mast cells. Although the ligands for PIR-A and PIR-B remain unknown, recent studies on PIR-B-deficient mice have provided us with valuable insight into the physiological significance of PIR-B, particularly in its regulatory role in balancing the humoral immune response.
KW - Autoimmunity
KW - B cell
KW - Dendritic cell
KW - Hypersensitivity
KW - Mast cell
KW - Th2 response
UR - http://www.scopus.com/inward/record.url?scp=3142630106&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=3142630106&partnerID=8YFLogxK
U2 - 10.1111/j.1440-1592.2004.00327.x
DO - 10.1111/j.1440-1592.2004.00327.x
M3 - Review article
AN - SCOPUS:3142630106
SN - 1323-8930
VL - 53
SP - 93
EP - 99
JO - Allergology International
JF - Allergology International
IS - 2
ER -