1.
J Neuroimmunol
; 120(1-2): 103-11, 2001 Nov 01.
Artigo
em Inglês
| MEDLINE
| ID: mdl-11694325
RESUMO
The monoclonal Lewis rat skeletal muscle cell line, LE1, responded to the acetylcholine receptor (AChR)-reactive antibody mAb35 by up-regulating levels of mRNA for inducible nitric oxide synthase (iNOS/NOS-II), followed by levels of NO. Interferon-gamma (IFN-gamma) and interleukin-1 (IL-1) were also each capable of inducing iNOS message, and synergistically with mAb35. Finally, myocyte-derived NO was implicated as a possible source of immunomodulation in experimental autoimmune myasthenia gravis (EAMG), as shown by the ability of the culture fluids from IFN-gamma-activated LE1 cells to inhibit the proliferation of AChR-reactive T cells.