![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center at Tufts University, Boston, MA
2To whom correspondence should be addressed. E-mail: simin.meydani{at}tufts.edu.
KEY WORDS: • vitamin E • vitamin A • tocopherol • immunoediting
The cancer immunosurveillance or the more recently modified cancer immunoediting hypothesis (1) proposes that the immune system, through a 2-way interaction with tumors, is an important determinant of host resistance to cancer. Based on this hypothesis, supported by studies using transgenic and immunodeficient animal models, as well as in tumor-bearing human subjects, the ability of the immune cells to recognize and destroy tumors or resist tumor-induced suppression is critical in determining tumor prognosis.
Fat-soluble vitamins are needed for maintaining optimal function of innate and adaptive immune cells. They may contribute to improving the immune response to tumors by (1) increasing tumor antigenecity, (2) enhancing the effector function of innate and adaptive immunity and their interaction, and (3) reducing production of immunosuppressive factors by tumors. Deficiency of vitamins A and E have been shown to impair CD4+ and CD8+ T cell mediated effector function, as well as the activity of the natural killer (NK) cells (2). In nontumor bearing hosts, supplementation with more than the recommended level of vitamin E has been shown to improve T cell-mediated function, including their ability to go through cell-cycle division and to produce IL-2 and INF-
(3–6). Furthermore, vitamin E supplementation was shown to reduce production of prostaglandin E2, a T cell suppressor factor produced by macrophages (7). Improvement in T cell function and NK cell activity has also been demonstrated in animal models and in elderly human subjects (8,9). Few studies, however, have evaluated the effect of fat-soluble vitamins on the immune response of a tumor-bearing host or on tumor-specific immune responses. Recently, supplementation with vitamin E-10 was shown to improve T cell function in cancer patients.
In summary, evidence from studies in nontumor-bearing animals and humans, as well as in limited reports from cancer patients, suggests that fat-soluble vitamins might be effective in improving immune response to tumors. Further research is needed to determine the efficacy of fat-soluble vitamins in improving tumor-specific immunity in normal and immunodeficient hosts. These studies should address all aspects of the immune response to tumors, i.e., tumor antigenicity, reduction of suppressor factors produced by tumors, and improving tumor-specific innate and adaptive immunity.
FOOTNOTES
1 Published in a supplement to The Journal of Nutrition. Presented during a workshop entitled: "Immunonutrition: Enhancing Tumoricidal Cell Activity," held in Bethesda, MD, March 23, 2005. This workshop was sponsored by the Division of Cancer Prevention, NCI, NIH, DHHS. Guest editors for the supplement publication were Susan S. Percival, John A. Milner, and Christopher A. Jolly. Guest Editor Disclosure: Susan S. Percival: no relationships to disclose; John A. Milner: no relationships to disclose; Christopher A. Jolly: received reimbursement for travel expenses from NCI. 
LITERATURE CITED
1. Dunn GP, Bruce AT, Ikeda H, Old LJ, Schreiber RD. Cancer immunoediting: from immunosurveillance to tumor escape. Nat Immunol. 2002;3(11):991-998.[Medline]
2. Meydani SN, Fawzi WW, Han SN. The effect of vitamin A deficiencies (E and A) and supplementation of infection and immune response. Suskind RM Tontisirin K eds. The effect of vitamin A deficiencies (E and A) and supplementation of infection and immune response. Nutrition, immunity, and infection in infants and children. :213-241 Williams and Wilkins Philadelphia: Lippincott.
3. Meydani SN, Leka LS, Fine BC, Dallal GE, Keusch GT, Singh MF, Hamer DH. Vitamin E and respiratory tract infections in elderly nursing home residents: a randomized controlled trial. J Am Med Assos. 2004;292(7):828-836.
4. Meydani SN, Meydani M, Blumberg JB, Leka LS, Siber G, Loszewski R, Thompson C, Pedrosa MC, Diamond RD, Stollar BD. Vitamin E supplementation and in vivo immune response in healthy elderly subjects. A randomized controlled trial. J Am Med Assoc. 1997;277(17):1380-1386.[Abstract]
5. Adolfsson O, Huber BT, Meydani SN. Vitamin E-enhanced IL-2 production in old mice: naive but not memory T cells show increased cell division cycling and IL-2-producing capacity. J Immunol. 2001;167(7):3809-3817.
6. Han SN, Wu D, Ha WK, Beharka A, Smith DE, Bender BS, Meydani SN. Vitamin E supplementation increases T helper 1 cytokine production in old mice infected with influenza virus. Immunology. 2000;100(4):487-493.[Medline]
7. Wu D, Mura C, Beharka AA, Han SN, Paulson KE, Hwang D, Meydani SN. Age-associated increase in PGE2 synthesis and COX activity in murine macrophages is reversed by vitamin E. Am J Physiol. 1998;275:C661-C668.
8. Santos MS, Leka LS, Ribaya-Mercado JD, Russell RM, Meydani M, Hennekens CH, Gaziano JM, Meydani SN. Short- and long-term beta-carotene supplementation do not influence T cell-mediated immunity in healthy elderly persons. Am J Clin Nutr. 1997;66:917-924.
9. Santos MS, Gaziano JM, Leka LS, Beharka AA, Hennekens CH, Meydani SN. Beta-carotene-induced enhancement of natural killer cell activity in elderly men: an investigation of the role of cytokines. Am J Clin Nutr. 1998;68(1):164-170.[Abstract]
10. Malmberg KJ, Lenkei R, Petersson M, Ohlum T, Ichihara F, Glimelius B, Frodin JE, Masucci G, Kiessling R. A short-term dietary supplementation of high doses of vitamin E increases T helper 1 cytokine production in patients with advanced colorectal cancer. Clin Cancer Res. 2002;8(6):1772-1778.
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||
