Zauli G, Catani L, Gibellini D, Re M C, Vianelli N, Colangeli V, Celeghini C, Capitani S, La Placa M
Institute of Human Anatomy, University of Ferrara, Italy.
Br J Haematol. 1996 Mar;92(3):711-7. doi: 10.1046/j.1365-2141.1996.367904.x.
Glycoproteic (GP) IIb/IIIa+ megakaryocytic cells were purified from the bone marrow (BM) of 15 HIV-1 seropositive thrombocytopenic patients, eight HIV-1 seronegative patients affected by immune thrombocytopenic purpura (ITP) and 14 HIV-1 seronegative normal donors. The presence of apoptosis was evaluated in freshly isolated GPIIb/IIIa+ cells by flow cytometry after propidium iodide staining and electron microscopy. GPIIb/IIIa+ cells from HIV-1 seropositive thrombocytopenic patients showed a significant (P < 0.0001) increase of apoptosis with respect to both HIV-1 seronegative ITP patients and normal donors. Moreover, the degree of apoptosis in bone marrow GPIIb/IIIa+ cells purified from HIV-1 seropositive thrombocytopenic patients was inversely (P < 0.01) related to the count of circulating platelets, whereas it did not show any significant correlation with the absolute number of circulating CD4 T cells, the CD4/CD8 ratio or the presence of proviral gag DNA sequences. Therefore neither an advanced stage of HIV-1 disease nor a direct infection with HIV-1 seems to play a primary role in the impaired survival of BMGPIIb/IIIa+ megakaryocytic cells. These findings strengthen the notation that, besides the immune targeting of peripheral platelets, an impairment of the bone marrow megakaryocyte compartment may also contribute to the pathogenesis of HIV-1 related thrombocytopenia.
从15例HIV-1血清阳性血小板减少患者、8例受免疫性血小板减少性紫癜（ITP）影响的HIV-1血清阴性患者以及14例HIV-1血清阴性正常供者的骨髓（BM）中纯化糖蛋白（GP）IIb/IIIa+巨核细胞。通过碘化丙啶染色后的流式细胞术和电子显微镜评估新鲜分离的GPIIb/IIIa+细胞中凋亡的存在情况。与HIV-1血清阴性ITP患者和正常供者相比，HIV-1血清阳性血小板减少患者的GPIIb/IIIa+细胞凋亡显著增加（P<0.0001）。此外，从HIV-1血清阳性血小板减少患者纯化的骨髓GPIIb/IIIa+细胞中的凋亡程度与循环血小板计数呈负相关（P<0.01），而与循环CD4 T细胞的绝对数量、CD4/CD8比值或前病毒gag DNA序列的存在无显著相关性。因此，HIV-1疾病的晚期阶段或HIV-1的直接感染似乎都不是BM GPIIb/IIIa+巨核细胞生存受损的主要原因。这些发现强化了这样一种观点，即除了外周血小板的免疫靶向作用外，骨髓巨核细胞区室的损伤也可能导致HIV-1相关血小板减少的发病机制。
