The acetylcholine receptor (AChR) deficit in the neuromuscular junctions leads to myasthenia gravis (MG). MG is primarily an antibody mediated autoimmune disease. However, the effector role of CD8+T cells in the development of EAMG has not been studied extensively Depletion of CDS cells in rat EAMG partially prevented the development of EAMG, suggesting an effector role for CDS cells. Initial studies performed in a conventional animal facility, depletion of CDS cells failed to suppress the mouse model of EAMG. In this study we housed the C57BL6 mice in microisolator cages in a viral antibody free barrier facility. We depleted CD 8+T cells by injecting monoclonal anti-CD8 antibody into B6 mice three days prior to immunization with Torpedo AChR in CFA. Only 4 of 15(26%) CDS cell depleted mice showed incidence of EAMG as compared to 8 of 15(53%) rat Ig treated; and 9 of 15(60%) PBS treated mice. The difference in clinical EAMG incidence between the CDS cell depleted and the control mice was significant (p- 0.05). Also the serum y-lFN levels were lower and serum IL-4,and IL-6 levels were higher in CDS depleted than in control groups. Thus CDS cell depletion shifts Thl profile to Th2. These Ereliminary findings suggest a possible effector role for CDS cells in AMG, either CDS cells are directly destroying post synaptic AChR or through the generation of pro-inflammatory cytokines.
|Original language||English (US)|
|State||Published - Dec 1 1996|
ASJC Scopus subject areas
- Molecular Biology