Vitamin D affects B cell function

Background:While vitamin D is increasingly recognized as a potential immune regulator of MSdisease activity, its impact on B lymphocytes, however, remains ill-defined.
Methods: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).
Results: B cells from MS patients with 25(OH)D serum levels < 20 ng/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.
Conclusion: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.

As MS becomes a B cell disease, why not see what everything does on B cell function. This study looks at vitamin D and B cell function and  if you have low vitamin D levels in the blood these are low in the brain and you have more B cell activity.

This study suggests that vitamin D plays a role in regulating humoral immunity and suggest a scenario in which low 25(OH)D levels in peripheral blood and CSF act together to facilitate the intrathecal accumulation of blood-derived, antigen-experienced, post-switched memory B cells. Once they have entered the CSF, their proliferative potency is enhanced and their subsequent differentiation into antibody-secreting effector cells promoted. As a consequence, hypovitaminosis D might contribute to augmenting MS disease activity in the target organ thus supporting a potential benefit of vitamin D supplementation in MS.

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