TY - JOUR
T1 - The presence of chemokine receptor (CCR5, CXCR3, CCR3)-positive cells and chemokine (MCP-1, MIP-1α, MIP-1β, IP-10)-positive cells in human periapical granulomas
AU - Kabashima, Hiroaki
AU - Yoneda, Masahiro
AU - Nagata, Kengo
AU - Hirofuji, Takao
AU - Ishihara, Yoshihisa
AU - Yamashita, Megumi
AU - Maeda, Katsumasa
N1 - Funding Information:
This work was in part supported by a Grants-in Aid for Scientific Research 13672189 from the Ministry of Education, Science, Sports and Culture of Japan.
PY - 2001
Y1 - 2001
N2 - The infiltration of leukocytes into inflammation sites such as observed in human periapical granulomas is considered to be mediated by chemotactic factors. In this study, we examined the presence of chemokine- and chemokine receptor-positive cells in samples obtained from human subjects by means of immunohistochemical methods. Macrophage chemotactic protein-1 (MCP-1), macrophage inflammatory protein (MIP)-1α, MIP-1β and IFN-inducible protein 10 (IP-10)-producing cells were present in periapical granulomas. In addition, chemokine receptor CCR3-, CCR5-, and CXCR3-positive cells were also present. In contrast, no factor expression was observed in clinically healthy periodontal ligament, serving as a negative control. Our findings suggest that these chemokines are responsible for modulating the process of disease, such as human apical periodontitis.
AB - The infiltration of leukocytes into inflammation sites such as observed in human periapical granulomas is considered to be mediated by chemotactic factors. In this study, we examined the presence of chemokine- and chemokine receptor-positive cells in samples obtained from human subjects by means of immunohistochemical methods. Macrophage chemotactic protein-1 (MCP-1), macrophage inflammatory protein (MIP)-1α, MIP-1β and IFN-inducible protein 10 (IP-10)-producing cells were present in periapical granulomas. In addition, chemokine receptor CCR3-, CCR5-, and CXCR3-positive cells were also present. In contrast, no factor expression was observed in clinically healthy periodontal ligament, serving as a negative control. Our findings suggest that these chemokines are responsible for modulating the process of disease, such as human apical periodontitis.
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U2 - 10.1006/cyto.2001.0947
DO - 10.1006/cyto.2001.0947
M3 - Article
C2 - 11683586
AN - SCOPUS:0036059248
VL - 16
SP - 62
EP - 66
JO - Cytokine
JF - Cytokine
SN - 1043-4666
IS - 2
ER -
