The active metabolite of vitamin D (1,25(OH)2D3) is an important modulator of the immune system. 1,25(OH)2D3 treatments, completely block the development of at least two different experimental autoimmune diseases. We show here that 1,25(OH)2D3 treatments prolong transplant graft survival for longer then cyclosporin A. Paradoxically, 1,25(OH)2D3 treatments do not compromise the ability of the host to fight a fungal or viral infection. Furthermore, cyclosporin A causes bone loss while 1,25(OH)2D3 actually increases bone mass. Thus, the use of 1,25(OH)2D3 and its analogs increase transplant survival while avoiding bone loss and opportunistic infections, two important disadvantages of the most widely used anti-transplant rejection drugs. The mechanism of action underlying 1,25(OH)2D3 regulation of the immune system is presently under investigation and will be discussed. Deletion of cytotoxic T cells has been eliminated as a possibility; instead the significance of 1.25(OH)2D3 mediated increases in the anti-inflammatory cytokines IL-4 and TGF-31 are being pursued.
|Original language||English (US)|
|State||Published - Mar 20 1998|
All Science Journal Classification (ASJC) codes
- Molecular Biology