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J Neuroimmunol. 2016 May 15;294:18-26. doi: 10.1016/j.jneuroim.2016.03.011. Epub 2016 Mar 23.

Hypovitaminosis D upscales B-cell immunoreactivity in multiple sclerosis.

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Department of Neurology, University Hospital of Heidelberg, Germany.
Department of Neurology, University Hospital of Heidelberg, Germany. Electronic address:



While vitamin D is increasingly recognized as a potential immune regulator of MS disease activity, its impact on B lymphocytes, however, remains ill-defined.


We assessed the impact of vitamin D on B-cell proliferation and cytokine secretion ex vivo and screened for effects of hypovitaminosis D and vitamin D supplementation on the compartmentalized distribution of B-cell subtypes in peripheral blood and cerebrospinal fluid (CSF) from patients with relapsing remitting MS (n=95) and various neurologic and healthy controls (n=57).


B cells from MS patients with 25(OH)D serum levels <20ng/ml, displayed enhanced immunoreactivity ex vivo as a consequence of more vigorous responses of CD27(+) memory phenotypes. Immune responses decreased when B cells from either source were co-cultured in the presence of vitamin D or when retesting B cells from MS patients after prolonged supplementation with vitamin D. Hypovitaminosis D was detectable in the serum of 40/95 MS patients, correlated with decreased vitamin D concentrations in CSF and with higher disease activity, and was paralleled by intrathecal accumulation of CD27(+) B-cell subtypes and plasma cells.


B-cell immunoreactivity is attenuated by vitamin D. Our finding that vitamin D deficiency affects the intrathecal compartment and coincides with increased frequencies of effector B-cell subtypes in the CSF suggests that hypovitaminosis D might contribute to augmenting disease activity in the target organ and supports a potential benefit of vitamin D supplementation in MS.


B lymphocytes; B-cell immunoreactivity; Cerebrospinal fluid; Hypovitaminosis D; Multiple sclerosis; Vitamin D

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