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Astaxanthin, a Carotenoid without Vitamin A Activity, Augments Antibody Responses in Cultures Including T-helper Cell Clones and Suboptimal Doses of Antigen1,2,

Harumi Jyonouchi*,3, Sining Sun*, Yoshifumi Tomita{dagger} and Myron D. Gross{ddagger}

* Department of Pediatrics, School of Medicine {ddagger} Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis, MN 55455 {dagger} Laboratory of Animal Nutrition and Biochemistry, Animal Science Division, Department of Agriculture, Miyazaki University, Miyazaki, Japan 889-21

Astaxanthin, a carotenoid without vitamin A activity, enhances T-dependent antigen (Ag)-specific humoral immune responses. We examined carotenoid actions on T-helper (Th) cell activity in a direct manner with reconstitution experiments; spleen Th cells were replaced with Ag-specific Type 1 and Type 2 (Th1 and Th2) Th cell clones. The Ag for the Th1 and Th2 clones were pigeon cytochrome C and rabbit {gamma}-globulin, respectively. Astaxanthin and ß-carotene augmented the number of IgM antibody (Ab)-secreting cells when unprimed B cells were incubated with Th clones and stimulated with suboptimal doses of Ag specific for each Th clone. The number of IgG Ab-secreting cells were greater with use of in vivo primed B cells than with unprimed B cells in both Th clones. Astaxanthin but not ß-carotene augmented the number of IgG Ab-secreting cells when primed B cells and Th cell clones were stimulated with suboptimal doses of Ag specific for each Th clone. In the presence of optimal doses of Ag for each Th clone, neither carotenoid augmented the number of Ab-secreting cells. Astaxanthin and ß-carotene may enhance the actions of both Th1 and Th2 cells for humoral immune responses with suboptimal Ag challenges; certain carotenoids may help maintain Ag-mediated immune responses at optimal levels.


KEY WORDS: • T-dependent antibody production • murine T-helper cell clones • astaxanthin • ß-carotene • antibody-secreting cells

1 Supported partly by AI-25066 (NIH) and by a grant from Nikken Sohonsha (Gifu, Japan) (to H. Jyonouchi).

2 The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.

3 To whom correspondence and reprint requests should be addressed at: Division of Immunology, Department of Pediatrics, University of Minnesota, Box 610, UMHC, 420 Delaware Street S.E., Minneapolis, MN 55455.

Manuscript received 27 January 1995. Revision accepted 8 June 1995.




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