Endocrinology published online (October 16) a study done by Alexander Misharin, et al, of the UCLA school of Medicine in LA . In the introduction, the authors state:
It is now well-recognized that, in addition to its role in skeletal homeostasis, vitamin D plays a role in both innate and adaptive immunity (reviewed in 1). The vitamin D receptor is expressed on monocytes and activated lymphocytes (2) and the biologically active metabolite of vitamin D [1,25 dihydroxyvitamin D3, 1,25(OH)2D3] is a potent modulator of T cell responses (3). Because of this activity, the immunological effects of vitamin D have been the subject of intense investigation in animal models of autoimmune disease.However, the authors had a "surprise" conclusion:
The continuing hyperthyroid state in vitamin D deprived BALB/c mice could not be attributed to any immunological difference (as described above)...For these reasons, it seems likely that persistent hyperthyroidism can only be attributed to a difference in the sensitivity to TSAb of the thyroid in BALB/c mice on deficient vitamin D diet.Although the research was done on mice, "vitamin D may have similar effects in humans".
A. Misharin, M. Hewison, C.-R. Chen, V. Lagishetty, H. A. Aliesky, Y. Mizutori, B. Rapoport, S. M. McLachlan (2008). Vitamin D deficiency modulates Graves' hyperthyroidism induced in BALB/c mice by thyrotropin receptor immunization Endocrinology DOI: 10.1210/en.2008-1191