Modulation of the humoral immune response by antibody-mediated antigen targeting to complement receptors and Fc receptors.
Modulation of the humoral immune response by antibody-mediated antigen targeting to complement receptors and Fc receptors.
复制标题
通过抗体介导的抗原靶向补体受体和 Fc 受体来调节体液免疫反应。
DOI:
10.4049/jimmunol.162.6.3125
复制
发表时间:
1999
影响因子:
4.4
通讯作者:
Wouter L. W. Hazenbos
中科院分区:
文献类型:
--
作者:
Dana C. Baiu;J. Prechl;A. Tchorbanov;Hector Molina;A. Erdei;A. Sulica;Peter J. A. Capel;Wouter L. W. Hazenbos
During an ongoing immune response, immune complexes, composed of Ag, complement factors, and Igs, are formed that can interact with complement receptors (CRs) and IgG Fc receptors (Fc gamma R). The role of CR1/2 and Fc gamma R in the regulation of the immune response was investigated using OVA that was chemically conjugated to whole IgG of the rat anti-mouse CR1/2 mAb 7G6. FACS analysis using the murine B cell lymphoma IIA1.6 confirmed that the 7G6-OVA conjugate recognized CR1/2. Incubating IIA1.6 cells with 7G6-OVA triggered tyrosine phosphorylation and Ag presentation to OVA-specific T cells in vitro. Immunizing mice with 7G6-OVA at a minimal dose of 1 microgram i.p. per mouse markedly enhanced the anti-OVA Ig response, which was primarily of the IgG1 isotype subclass. The 7G6-OVA did not enhance the anti-OVA response in CR1/2-deficient mice. OVA coupled to an isotype control Ab induced a considerably lower anti-OVA response compared with that induced by OVA alone, suggesting inhibition by interaction between the Fc part of the Ab and the inhibitory Fc gamma RIIb on B cells. This findings was supported by the observation that IIA1.6 cells which were incubated with 7G6-OVA lost the ability to present Ag upon transfection with Fc gamma RIIb. In sum, 7G6-conjugated OVA, resembling a natural immune complex, induces an enhanced anti-OVA immune response that involves at least CR1/2-mediated stimulation and that may be partially suppressed by Fc gamma RIIb.
登录
查看更多内容
影响因子:
4.4
作者:
Y. Kozono;Y. Kozono;R. Abe;H. Kozono;Robert G. Kelly;T. Azuma;V. Holers
通讯作者:
Y. Kozono;Y. Kozono;R. Abe;H. Kozono;Robert G. Kelly;T. Azuma;V. Holers
DOI:
--
发表时间:
1997
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Mongini,PK;Vilensky,MA;Highet,PF;Inman,JK
通讯作者:
Inman,JK
DOI:
--
发表时间:
1996
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Fischer,MB;Ma,M;Goerg,S;Zhou,X;Xia,J;Finco,O;Han,S;Kelsoe,G;Howard,RG;Rothstein,TL;Kremmer,E;Rosen,FS;Carroll,MC
通讯作者:
Carroll,MC
DOI:
--
发表时间:
1986
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Jones,B;Tite,JP;JanewayJr,CA
通讯作者:
JanewayJr,CA
DOI:
--
发表时间:
1991
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Thyphronitis,G;Kinoshita,T;Inoue,K;Schweinle,JE;Tsokos,GC;Metcalf,ES;Finkelman,FD;Balow,JE
通讯作者:
Balow,JE