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  • Back to Therapeutic Vitamin D…The T-cell Link

     IveyTech updated 1 month, 1 week ago 1 Member · 4 Posts
  • IveyTech

    May 8, 2021 at 8:48 am

    EXCERPT from March 2010 Scientific American:

    In order for T cells to become active members of the body’s immune system, they must transition from so-called “naive” T cells into either killer cells or helper cells (which are charged with “remembering” specific invaders). And, if ample vitamin D is not around, the T cells do not make that crucial transition, a group of researchers led by Carsten Geisler, head of the Department of International Health, Immunology and Microbiology at the University of Copenhagen, found. They draw this conclusion based on their experiments with isolated naïve human T cells.

    “When a T cell is exposed to a foreign pathogen, it extends a signaling device of ‘antenna’ known as a vitamin D receptor, with which it searches for vitamin D,” Geisler said in a prepared statement. If there is an inadequate vitamin D level, he noted, “they won’t even begin to mobilize.”


  • IveyTech

    May 8, 2021 at 8:54 am

    <div>Here is a useful list in this link to the T-cell/Vitamin D synergistic relationship</div><div>



  • IveyTech

    May 8, 2021 at 9:09 am

    <div>Here is another list on the relationship of Vitamin D to the immune system function</div><div>



  • IveyTech

    May 8, 2021 at 9:26 am



    Since the mechanisms of immunity against COVID-19 are presently incompletely understood, we will describe several processes by which vitamin D boosts immunity against viral infections more generally, which may also be applicable to SARS-CoV-2. In general, innate immune cells, macrophages, first phagocytize pathogens and then communicates with naïve T cells to induce activation. The activated naïve T cell converts into either T helper 1 (Th1) or Th2 cells. With vitamin D deficiency, the adaptive immune response shifts towards the Th1 direction, which may thereby cause the hyper-inflammation/ cytokine storm since these cells release the inflammatory cytokines, IL-2 and IL-21. Moreover, when Th1 cells are activated, they, in turn, activate macrophages by releasing IFN-γ, which leads to production of IL-6, IL-1, IL-8, and TGF-β, the latter of which activates Th17 cells to secrete IL-17. IL-1, IL-6, IL-8, IL-17 and IL-21 are all important pro-inflammatory cytokines (Fig. 2). Vitamin D has been found to suppress the adaptive immune response by decreasing T cell proliferation <sup>[162]</sup><sup>, </sup><sup>[163]</sup>. In experimental mouse models, down-regulated adaptive immune responses mediated by Th1 cells were observed, as well as decreases in the levels of IFN-γ, IL-6, IL-2, and TNF-α <sup>[164]</sup><sup>, </sup><sup>[165]</sup>. Moreover, down-regulation of Th1 cell-response cytokines, especially IFNγ, as well as stimulation of Th2-cell responses, were found <sup>[163]</sup><sup>, </sup><sup>[166]</sup>.

    The Th2 cell type immune response is anti-inflammatory and thus works to control inflammation. This is effected by the secretion of IL-4, IL-5 and IL-10 by the Th2 cells. IL-4 and IL-5 activate B cells to proliferate and mature, which in turn release antibodies against pathogens. By contrast, IL-10 suppresses the activation of Th1 and the expression of major histocompatibility complex II (MHC-II) in macrophages, which reduces inflammation. IL-10 also results in a lower degree of communication between macrophages and naïve T cells. All of these effects prevent the over-activation of adaptive immunity that is hyper-inflammation. Generally, the COVID-19 patient’s immune system shifts to the Th2 phenotype in most cases <sup>[84]</sup> which helps with a quick control of the disease. Unfortunately, approximately 15–20% of COVID-19 cases undergo severe disease. Clinical data compiled by Daneshkhah and colleagues <sup>[167]</sup> indicate that vitamin D deficiency in severe COVID-19 patients is 34% (age ≥ 60 years), 22% (20 years ≤ age < 40 years), and 21% (40 years ≤ age < 60 years) more frequent than in patients with normal vitamin D levels. With the correct level of vitamin D, the immune system shifts to the Th2 phenotype direction that inhibits the production of pro-inflammatory cytokines <sup>[164]</sup><sup>, </sup><sup>[165]</sup>, resulting in an anti-inflammatory reaction and a control of the otherwise overreaction of the immune system in chronic-relapsing experimental allergic encephalomyelitis <sup>[168]</sup><sup>, </sup><sup>[169]</sup>. Furthermore, a recent experimental study has shown that vitamin D can induce the production of more anti-inflammatory cytokines, such as IL-10, which in turn is expected to reduce the severity of the disease <sup>[170]</sup>. However, with vitamin D deficiency or insufficiency, the body’s immune system shifts towards the Th1 direction and hyper-inflammation/cytokine storm might occur <sup>[171]</sup>. Furthermore, vitamin D governs T-cell differentiation by regulating antigen-presenting dendritic cells, causing them to reduce the synthesis of IL-12 that promotes Th1-cell responses <sup>[172]</sup><sup>, </sup><sup>[173]</sup>. Vitamin D also exerts an important effect on the activity of the immune system by decreasing Th17-cell responses and the differentiation of naive T cells into Th17 type cells which decreases secretion of several pro-inflammatory cytokines, including IL-6, IL-17 and IL-23 <sup>[174]</sup><sup>, </sup><sup>[175]</sup>. In addition, vitamin D decreases the synthesis of IL-12 and simultaneously increases the production of IL-10 by dendritic cells (DCs) <sup>[170]</sup>. Overall, thus, these results indicate that vitamin D moves the adaptive immune response from a Th1- to a Th2-phenotype <sup>[168]</sup><sup>, </sup><sup>[169]</sup>, decreases the differentiation of naïve T cells into Th17 cells <sup>[174]</sup><sup>, </sup><sup>[176]</sup> and enhances the T regulatory type response, leading to an inhibition of inflammatory processes <sup>[177]</sup><sup>, </sup><sup>[178]</sup><sup>, </sup><sup>[179]</sup><sup>, </sup><sup>[180]</sup>. In this way, vitamin D might help in the treatment of COVID-19 by preventing the cytokine storm and subsequent ARDS which is a common cause of mortality <sup>[8]</sup>.

    9. Vitamin D deficiency and severity of COVID-19

    The major cause of vitamin D deficiency is insufficient exposure to sunlight <sup>[181]</sup>, with also some dependency of basal metabolic index (BMI) and aging <sup>[182]</sup><sup>, </sup><sup>[183]</sup>. Patients with chronic kidney and liver diseases also have vitamin D deficiency <sup>[184]</sup>. For more than a century, vitamin D deficiency has been suggested to increase the susceptibility to RTI. The increased risk of RTIs in children with nutritional rickets <sup>[185]</sup> and vitamin D is considered of importance in the treatment of tuberculosis <sup>[186]</sup>. An observational study of 9548 adults aged 50 to 75 years in Germany has shown that vitamin D insufficiency and deficiency strongly increases respiratory disease mortality <sup>[187]</sup>. Consistent with this observational data, several randomized clinical trials show a strong link between vitamin D deficiency and COVID-19 severity and mortality, and that supplementation could reduce the severity <sup>[128]</sup><sup>, </sup><sup>[129]</sup><sup>, </sup><sup>[132]</sup>. Recent studies have provided further evidence that vitamin D is an important regulator of human immune function, perhaps, as described above, as a result of its stimulation of the innate immune response […] <sup>[112]</sup><sup>, </sup><sup>[113]</sup><sup>, </sup>

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0 of 0 posts June 2018