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Objective: TO verify the antigen association ofMAF-J6-1 receptor with M-CSFR and to further studythe role of M-CSF and its receptor mediated juxtacrinein promoting leukemic cell proliferation. Methods:Monoclonal antibody (McAb) of MAF-J6-1R RE2 andpolyclonal antibody (PolyAb) of rhM-CSFR wereprepared. The specificity of McAb RE2 to M-CSFR wasconfirmed by indirect ELISA, cross-neutralizing assaywith J6-1 cell colony formation and neutralization testby ELISA. Results: The reactive activity of punt’iedRE2 to M-CSFR was over 1: 16000. The inhibitoryactivity of M-CSFR and MAF-J6-IR could be blockedby RE2 and anti-M-CSFR antibody. The reactivity ofRE2 to M-CSFR could be reduced by M-CSFR.Conclusion: The specificity of RE2 to M-CSFR wasconfirmed and the antigen association of MAF-J6-1Rwith M-CSFR was proved. It suggests that M-CSF andits receptor mediated auto-juxtacrine stimulation couldbe an operative mechanism in either leukemia or nonhematological malignancies.
Objective: TO verify the antigen association ofMAF-J6-1 receptor with M-CSFR and to further studythe role of M-CSF and its receptor mediated juxtacrinein promoting leukemic cell proliferation. Methods:Monclonal Antibody (McAb) of MAF-J6-1R RE2 Andpolyclonal antibody (PolyAb) of rhM-CSFR wereprepared. The specificity of McAb RE2 to M-CSFR wasconfirmed by indirect ELISA, cross-neutralizing assaywith J6-1 cell colony formation and neutralization testby ELISA. Results: The reactive activity of punt’iedRE2 to M-CSFR was over 1: 16000. The inhibitory activity of M-CSFR and MAF-J6-IR could be blocked by RE2 and anti-M-CSFR antibody. The reactivity of RE2 to M-CSFR could be reduced by M-CSFR.Conclusion: The specificity of RE2 to M-CSFR was confirmed and the antigen association of MAF-J6-1Rwith M-CSFR was proved. It suggests that M-CSF andits receptor mediated auto-juxtacrine stimulation couldbe an operative mechanism in either leukemia or nonhematological malignancies.