Wilson A B, Lachmann P J, Coombs R R
Immunology. 1979 May;37(1):25-34.
The activation of C3, previously demonstrated to occur during the isolation of lymphocytes from rabbit blood, has been investigated further by in vitro exposure of blood and lymph node lymphocytes and thymocytes to autologous serum. Activated C3 deposited on the lymphoid cell-surface was detected by (i) anti-C3, (ii) immune adherence reaction, and (iii) blocking of receptors for C3. An affinity shown by guinea-pig erythrocytes for activated complement was also investigated. Using EGTA, which inhibits the classical complement pathway while leaving the alternative pathway unaffected, it was shown that either pathway may be activated by rabbit cells depending on the temperature of incubation. The classical pathway was triggered at 4 degrees, probably by the reaction of cold auto-antibodies with lymphoid cell-surface determinants. At 37 degrees, however, comlement activation followed the alternative pathway in a similar manner to that reported by other workers with human lymphoblastoid cell lines.
先前已证实在从兔血中分离淋巴细胞的过程中会发生C3激活,现通过将血液、淋巴结淋巴细胞和胸腺细胞体外暴露于自体血清中,对其进行了进一步研究。通过以下方法检测沉积在淋巴细胞表面的活化C3:(i)抗C3;(ii)免疫黏附反应;(iii)C3受体阻断。还研究了豚鼠红细胞对活化补体的亲和力。使用乙二醇双四乙酸(EGTA),它可抑制经典补体途径而不影响替代途径,结果表明,根据孵育温度,兔细胞可激活任一途径。经典途径在4℃时被触发,可能是冷自身抗体与淋巴细胞表面决定簇反应所致。然而,在37℃时,补体激活遵循替代途径,其方式与其他研究人员用人淋巴母细胞系报道的相似。