Antioxidants, and the Immune System

The proliferation of T and B cells, natural killer cells, and lymphokine activated killer cells that are required to mount an effective defense against pathogens and tumor cells appear to be inhibited markedly with age and upon exposure to oxidants. These effects can, in part, be counteracted in elderly individuals by dietary antioxidant supplementation. While the endogenous sources of oxidants that lead to the suppression of lymphocyte dependent immunity are not known, in vitro studies have demonstrated that polymorphonuclear leucocytes and macrophages, both can inhibit proliferation of various lymphocyte subpopulations through the production of reactive oxygen intermediates and the prostaglandin metabolite PGE2 as well as from nitric oxide.

This suggests that conditions that involve infiltration of polymorphonuclear leucocytes and macrophages (i.e., chronic inflammatory diseases), could result in compromised lymphocyte function. The suppressive effects of macrophages on mitogen induced lymphocyte proliferation can be reversed partially by thiol reagents, catalase or indomethacin, or by NG-monomethyl-L-arginine, a competitive inhibitor of nitric oxide synthesis.

The age associated decrease in cell mediated immunity may be due to a decreased level of certain small molecule antioxidant and antioxidant enzymes that accompany the aging process.

Calorie restriction, a dietary regimen that increases maximal lifespan in rodents also enhances T lymphocyte responsiveness possibly by slowing the rate of thymus involution and by boosting the level of cellular antioxidant defenses.