In adult humans, the thymus is involuted, which suggests that extrathymic differentiation of T-cell progenitors, peripheral expansion of mature T
cells, or both are the principal mechanisms of T-cell reconstitution after transplantation. Dreger et al17 showed a lack of naive CD45RA+ cells after AHSCT, suggesting that most circulating T cells after AHSCT in humans are activated memory CD45RO+ cells rather than naive T cells. The deficient numbers of naive T cells predict the inability to elicit immune responses against new antigens after AHSCT.
Prospective monitoring of CD4+ T cell subsets revealed that Tregs rapidly expanded and achieved normal levels by 9 months after HSCT, but Treg levels subsequently declined in patients with prolonged CD4+ lymphopenia.
Epidemiological studies have shown that a poor vitamin D status is associated with an increased risk of several diseases, including autoimmune diseases. The immune regulatory function of vitamin D is thought to have an important role in these associations. Cells of the adaptive immune system have shown to be direct targets of the vitamin D metabolites. Besides being direct targets, cells of the adaptive immune system express the enzymes involved in the metabolism of vitamin D, enabling them to locally convert 25(OH)D into its active metabolite 1,25(OH)2D. In this review, the effects of vitamin D on cells of the adaptive immune system are described. Experimental data in vitro show that vitamin D skews cells of the adaptive immune system toward a more tolerogenic status which might be exploited in the treatment of autoimmune diseases. However, it should be noticed that in vivo effects may differ from in vitro effects due to the cross-talk between different vitamin D sensitive cells, but data support the view that vitamin D is positively involved in maintaining or restoring immune homeostasis. Upcoming vitamin D supplementation trials will further elucidate the in vivo effects of vitamin D on the immune system and its potency to serve as an immune regulating agent in autoimmune diseases.
We speculate that the loss of axonal stabilizing and protective effects of MAG may contribute to the late axonal degeneration
seen in demyelinating diseases. Although MAG is not a component of compact myelin,MAG is known to be lost from oligodendrocytes
and Schwann cells that have undergone demyelination. There is a wealth of evidence that axons are liable to both prompt
and progressive late Wallerian-like degeneration after demyelination (Dyck, 1975; Trapp et al., 1998; Scherer, 1999; Berciano et
al., 2000; Krajewski et al., 2000; Bjartmar et al., 2003; Oh et al., 2004).
Stem Cells Provide Blank Slate
A team at Northwestern University’s Feinberg School of Medicine, led by Dr. Richard Burt, has been “resetting” the immune system of MS patients by transplanting their own immune stem cells.
In one study, eighteen of twenty-one MS patients with the relapsing-remitting form of the disease improved significantly for twenty-four months after the stem cell transplant, and none got worse.
Most patients with relapsing-remitting MS get progressively worse as irreversible damage to their neurons accumulates.
The procedure involves harvesting immune stem cells from the patient’s bone marrow, and then destroying the immune component of the bone marrow with chemotherapy. When the stem cells are transplanted, the patient develops a new immune system apparently free of disease.
“The stem cells are not immune cells,” Burt said. “They have to be educated. They have to differentiate and grow into immune cells. The reset [after transplantation] results in an immune system like a newborn child’s.”
Burt has applied this technique to other diseases, including type 1 diabetes, lupus, scleroderma, Crohn’s, and a form of vision loss known as autoimmune-related retinopathy and optic neuropathy syndrome, or ARRON.
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