EFFECTS OF C‐REACTIVE PROTEIN (CRP) ON PLATELET FUNCTION *

In 1930, Tillett and Francis’ observed that sera obtained from patients during acute febrile illnesses had the ability to precipitate with an extract of the pneumococcus, designated Fraction C (or C-substance) and later C-polysaccharide (CPS). TilIett, Goebel and Ave$ termed this material “C-precipitin” and Ash3 showed that it occurred in nonfebrile illnesses caused by both Gram-positive and Gram-negative bacteria. This material also was found in the sera of patients with rheumatic fever and other diseases of bacterial origin, and Abernethy and Francis4 observed that the C-substance could induce cutaneous reactions selectively in patients who had the C-precipitins in their sera. Abernethy and Avery‘ presented evidence that the C-precipitin was a protein (hence C-reactive protein or CRP) and demonstrated that calcium was required for it to react with the C-substance. They proposed that CRP was distinct from antibody because it occurred only during the acute stages of infection, occurred in a variety of infectious and noninfectious illnesses independent of the inciting agent, was present in the albumin rather than in the globulin fractions during precipitation with ammonium sulfate, and required calcium for precipitation when it was reacted with C-substance. MacLeod and Avery”’ extended these observations and purified the protein, demonstrating its immunologic specificity by both precipitation and complement fixation tests with antisera raised in rabbits to the purified material. Serum CRP then could be detected and quantified by precipitation with specific antisera, precipitation with the C-substance, or by calciumdependent capsular swelling reactions with appropriate strains of pneumococ-