Baum L L, Johnson B, Berman S, Graham D, Mold C
Immunology. 1987 May;61(1):93-9.
Anti-CRP and complement treatment of human peripheral blood lymphocytes significantly reduces natural killer (NK) cell-mediated cytotoxicity to K562 target cells as well as to MOLT-4 target cells. Although not all activity is eliminated by treatment of effector cells with antibody and complement, the reduction of NK function indicates that C-reactive protein (CRP) is present on a significant proportion of NK cells. Higher concentrations of anti-CRP or anti-CRP F(ab')2 fragments also reduce NK function; this suggests that CRP is not only present on these effector cells but may also play a role in NK-mediated killing. We initially suspected that CRP-ligand interactions might be involved in effector-target cell recognition. Several lines of evidence suggest that this is not the case. While F(ab')2 anti-CRP will block NK function, Fab anti-CRP will not, suggesting that the NK response is not impaired when surface CRP (S-CRP) is blocked but is only inhibited when the S-CRP is cross-linked and modulated. Neither CRP-C polysaccharide complexes (CRP-CPS) nor concentrations of CPS ranging from 0.1 microgram/ml to 200 micrograms/ml have any effect on NK cell-mediated killing. Treatment of target cells with a ligand for CRP or CRP prior to co-culture with NK effectors does not augment NK function. Single cell assays clearly demonstrate that high concentrations of anti-CRP have no effect on the formation of effector-target cell conjugates. Although these concentrations of anti-CRP do not block effector-target cell conjugation in the single cell assay, they do block the killing of conjugated target cells. In total, this evidence strongly suggests that although CRP appears to be involved in NK-mediated killing, it is not involved in effector-target cell-mediated recognition.
用人外周血淋巴细胞进行抗C反应蛋白（CRP）和补体处理，可显著降低自然杀伤（NK）细胞对K562靶细胞以及MOLT-4靶细胞的细胞毒性。尽管用抗体和补体处理效应细胞并不能消除所有活性，但NK功能的降低表明相当比例的NK细胞上存在C反应蛋白（CRP）。更高浓度的抗CRP或抗CRP F(ab')2片段也会降低NK功能；这表明CRP不仅存在于这些效应细胞上，还可能在NK介导的杀伤中发挥作用。我们最初怀疑CRP-配体相互作用可能参与效应细胞与靶细胞的识别。但有几条证据表明并非如此。虽然F(ab')2抗CRP会阻断NK功能，但Fab抗CRP则不会，这表明当表面CRP（S-CRP）被阻断时，NK反应并未受损，只有当S-CRP被交联和调节时才会受到抑制。CRP-C多糖复合物（CRP-CPS）以及浓度范围从0.1微克/毫升到200微克/毫升的CPS对NK细胞介导的杀伤均无任何影响。在用NK效应细胞共培养之前，用CRP的配体或CRP处理靶细胞并不会增强NK功能。单细胞分析清楚地表明，高浓度的抗CRP对效应细胞与靶细胞结合物的形成没有影响。尽管在单细胞分析中这些浓度的抗CRP不会阻断效应细胞与靶细胞的结合，但它们确实会阻断结合的靶细胞的杀伤。总的来说，这些证据有力地表明，尽管CRP似乎参与了NK介导的杀伤，但它并不参与效应细胞与靶细胞介导的识别。
