Barnhart D D, Gengozian N
Clin Exp Immunol. 1975 Sep;21(3):493-500.
Inoculation of S. oedipus marmosets with white blood cells and platelets from another species of marmosets, S. fuscicollis, led to an acute and fatal thrombocytopenia. Antibody in the recipients to the immunizing platelets was found by agglutination and indirect immunofluorescence; also, serum from the afflicted animals passively induced thrombocytopenia in S. fuscicollis marmosets. Similar inoculations of S. oedipus marmosets with platelet-free white blood cell preparations from the same donors were without any clinical effect; also, immunization with autologous, allogeneic (unrelated S. oedipus) or human platelets, did not cause the disease, even though antibody to the latter species of platelets, human, was formed in the recipients. Failure to detect antibody to autologous (or allogeneic) platelets in the afflicted animals suggests induction of a disease process similar to that of post-transfusion purpura,where it has been speculated that the thrombocytopenia results from the adherence of antigen (donor) antibody complexes to host platelets, leading to their destruction by the reticuloendothelial system. The severity and consistency of inducing the disease in the marmoset by an active immunization process suggests this system may serve as an excellent animal model for autoimmune diseases falling within the syndrome of idiopathic thrombocytopenic purpura in man.
用另一种狨猴——棕颈狨猴的白细胞和血小板接种普通狨猴，会导致急性致命性血小板减少症。通过凝集反应和间接免疫荧光法发现，受体中存在针对免疫血小板的抗体；此外，患病动物的血清能使棕颈狨猴被动诱发血小板减少症。用来自相同供体的无血小板白细胞制剂对普通狨猴进行类似接种，未产生任何临床效果；而且，用自体、同种异体（无关的普通狨猴）或人类血小板进行免疫，也不会引发该病，尽管受体中形成了针对后一种血小板（人类）的抗体。在患病动物中未能检测到针对自体（或同种异体）血小板的抗体，这表明诱发了一种类似于输血后紫癜的疾病过程，据推测，血小板减少症是由于抗原（供体）抗体复合物黏附于宿主血小板，导致其被网状内皮系统破坏所致。通过主动免疫过程在狨猴中诱发该病的严重性和一致性表明，这个系统可能是人类特发性血小板减少性紫癜综合征范围内自身免疫性疾病的优良动物模型。
