The anti-inflammatory role of the erythrocyte: impairment in the elderly

Human erythrocytes have significant anti-inflammatory capability. Via their complement receptor, CR1 (CD35), they function as the major carriers of immune complexes in the circulation and as a co-factor for factor-I in the cleavage of C3b and the resultant inactivation of C3- and C5-convertases. Erythrocytes of the elderly are defective in their control of C3- and C5-convertases and are thus defective in protecting the elderly from the inflammatory consequences of the activation of complement in the circulation. This defect stems from the reduced levels of CR1 and decay accelerating factor and from defective CR1 function. Erythrocytes of the elderly resemble senescent erythrocytes from young donors in that their CR1 can neither bind immune complexes nor function as a co-factor in the factor-I mediated cleavage of C3b. The erythrocytes of the elderly are defective in both promoting convertase decay and supporting C3b cleavage. The reduced levels and functional defects of erythrocyte CR1 should hamper the ability of the elderly individual to effectively clear the circulation of potentially inflammatory immune complexes as well as of micro-organisms which have bound complement via the alternative complement pathway. This defect in the ability to clear immune complexes and micro-organisms bearing C3b from the circulation should render the elderly individual susceptible to varied pathologies including infection, inflammation and concomitant damage to the vascular tissue commonly observed in the elderly.