Allo-immunization elicits CCR5 antibodies, SDF-1 chemokines, and CD8-suppressor factors that inhibit transmission of R5 and X4 HIV-1 in women

被引:31
作者
Wang, Y
Underwood, J
Vaughan, R
Harmer, A
Doyle, C
Lehner, T
机构
[1] Kings Coll London, Guys Kings & St Thomas Med Sch, Dept Tissue Typing, London SE1 9RT, England
[2] St Marys Hosp, Imperial Coll, Dept Gynaecol, Fac Med, London, England
[3] Kings Coll London, Guys Kings & St Thomas Med Sch, Peter Gorer Dept Immunobiol, London SE1 9RT, England
关键词
allo-immunization; HIV-1; chemokines; CCR5; antibodies; recurrent spontaneous abortion;
D O I
10.1046/j.1365-2249.2002.01936.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Studies in humans suggest that allo-immunization induces CC-chemokines, CD8-suppressor factors (SF) and anti-HIV immunity. Here we report that allo-immunization with unmatched leucocytes from partners of women with recurrent spontaneous abortion elicits specific antibodies to the CCR5 receptor. Such antibodies inhibit replication of M-tropic HIV-1 (R5) and MIP-1beta-mediated chemotaxis. These CCR5 antibodies were also found in the sera of multiparous women that were naturally immunized by semi-allogeneic fetal antigens. The specificity of these antibodies was demonstrated by adsorption with CCR5 transfected HEK-293 cells, a baculovirus CCR5 preparation and a peptide of the 2nd extra-cellular loop of CCR5. Allo-immunization also stimulated increased concentrations of the CXC chemokine, SDF-1alpha and CD8-SF that inhibit T-tropic HIV-1 (X4) replication. We suggest that allo- immunization may elicit (a) CC chemokines, CCR5 antibodies and CD8-SF that inhibit M-tropic HIV-1 infection and (b) the CXC chemokine SDF-1alpha and CD8-SF that inhibit T-tropic HIV-1 infection.
引用
收藏
页码:493 / 501
页数:9
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