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BioMed Research International
Volume 2013, Article ID 782067, 8 pages
Research Article

Supplementation with Natural Forms of Vitamin E Augments Antigen-Specific TH1-Type Immune Response to Tetanus Toxoid

1Pathology Division, Faculty of Medicine and Health, International Medical University, 126, Jalan Jalil Perkasa 19, Bukit Jalil, 57000 Kuala Lumpur, Wilayah Persekutuan, Malaysia
2Department of Nutrition, Malaysian Palm Oil Board, 6, Persiaran Institusi, Bandar Baru Bangi, 43000 Kajang, Selangor Darul Ehsan, Malaysia

Received 8 April 2013; Accepted 10 June 2013

Academic Editor: Udai P. Singh

Copyright © 2013 Ammu Kutty Radhakrishnan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


This study compared the ability of three forms of vitamin E [tocotrienol-rich fraction (TRF), alpha-tocopherol ( -T), and delta-tocotrienol ( -T3)] to enhance immune response to tetanus toxoid (TT) immunisation in a mouse model. Twenty BALB/c mice were divided into four groups of five mice each. The mice were fed with the different forms of vitamin E (1 mg) or vehicle daily for two weeks before they were given the TT vaccine [4 Lf] intramuscularly (i.m.). Booster vaccinations were given on days 28 and 42. Serum was collected (days 0, 28, and 56) to quantify anti-TT levels. At autopsy, splenocytes harvested were cultured with TT or mitogens. The production of anti-TT antibodies was augmented ( ) in mice that were fed with -T3 or TRF compared to controls. The production of IFN- and IL-4 by splenocytes from the vitamin E treated mice was significantly ( ) higher than that from controls. The IFN- production was the highest in animals supplemented with -T3 followed by TRF and finally -T. Production of TNF- was suppressed in the vitamin E treated group compared to vehicle-supplemented controls. Supplementation with -T3 or TRF can enhance immune response to TT immunisation and production of cytokines that promote cell-mediated (TH1) immune response.