同种免疫会引发CCR5抗体、SDF-1趋化因子和CD8抑制因子，这些会抑制R5和X4型HIV-1在女性体内的传播。
Allo-immunization elicits CCR5 antibodies, SDF-1 chemokines, and CD8-suppressor factors that inhibit transmission of R5 and X4 HIV-1 in women.
作者信息
Wang Y, Underwood J, Vaughan R, Harmer A, Doyle C, Lehner T
机构信息
Peter Gorer Department of Immunobiology, Guy's, King's and St Thomas' Medical School, King's College London, UK.
出版信息
Clin Exp Immunol. 2002 Sep;129(3):493-501. doi: 10.1046/j.1365-2249.2002.01936.x.
Abstract
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.
摘要
人体研究表明，同种免疫可诱导CC趋化因子、CD8抑制因子（SF）及抗HIV免疫力。在此我们报告，用反复自然流产女性伴侣的不匹配白细胞进行同种免疫，可引发针对CCR5受体的特异性抗体。此类抗体可抑制M嗜亲性HIV-1（R5）的复制及MIP-1β介导的趋化作用。在经半同种异体胎儿抗原自然免疫的经产妇血清中也发现了这些CCR5抗体。通过用CCR5转染的HEK-293细胞、杆状病毒CCR5制剂及CCR5第二个细胞外环的肽进行吸附，证实了这些抗体的特异性。同种免疫还刺激了抑制T嗜亲性HIV-1（X4）复制的CXC趋化因子SDF-1α和CD8-SF浓度升高。我们认为，同种免疫可能引发（a）抑制M嗜亲性HIV-1感染的CC趋化因子、CCR5抗体和CD8-SF，以及（b）抑制T嗜亲性HIV-1感染的CXC趋化因子SDF-1α和CD8-SF。
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