Figure 1. Pentameter structure of CRP, including calcium and phosphocholine binding sites. These sites enable CRP to recognize and bind to a variety of microorganisms, cellular debris, and nuclear material from damaged cells. Data from Kushner.
Figure 2. Key functions of CRP within the innate immune system include the ability to (1) recognize and bind to phosphocholine exposed in damaged cell walls and found in many bacteria, fungi, and parasites; (2) act like an opsonin, marking bacteria, damaged cell walls, and nuclear debris for phagocytosis; (3) bind to Cl, the first component of the classical pathway of the complement system that triggers phagocytic activity; and (4) bind to polymorphonuclear leukocytes (PMNs) and monocytes, which stimulate the production of inflammatory cytokines. Data from DuClos.
Figure 3. Stimulation and synthesis of positive acute-phase reactants during inflammation. Inflammation caused by infection or tissue damage stimulates the circulating inflammation-associated cytokines, including interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor (TNF)-. These cytokines stimulate hepatocytes to increase the synthesis and release of positive acute-phase proteins, including CRP. IL-6 is the major cytokine stimulus for CRP production.