Pathophysiological concentrations of CRP inhibited the in vitro clonal proliferation of CFU-C's. CRP inhibition was specific for normal CFU-C's committed to the mononuclear phagocyte lineage. Macrophage progenitor cells stimulated by an inflammatory response were unaffected by CRP. CFU-C's which were committed to the granulocyte lineage, those which gave rise to both macrophages and granulocytes, and erythroid progenitor cells were also not affected by CRP. Only macrophage CFU-C's that possessed Fc receptors and were in S-phase at the time of CRP exposure were susceptible to inhibition of colony formation. The data suggest that CRP functions as a regulator of the cellular composition of an inflammatory response.
|Original language||English (US)|
|Number of pages||11|
|Journal||The Journal of Laboratory and Clinical Medicine|
|State||Published - Jul 1982|
All Science Journal Classification (ASJC) codes
- Pathology and Forensic Medicine