Macrophage infiltration at the neuromuscular junction does not contribute to AChR loss and age-related resistance to EAMG.

Aged rats resistant to acetylcholine receptor loss in passive transfer experimental autoimmune myasthenia gravis (EAMG) do not reveal infiltrating macrophages at the neuromuscular junction (NMJ) as observed in susceptible rats. It was investigated whether this age-related resistance is due to impaired macrophage function in these aged rats. Reconstitution of aged rats with bone marrow from young donors did not lead to macrophage infiltration, nor did it abolish resistance to EAMG. Subsequently, it was investigated whether macrophages are a primary cause of acetylcholine receptor (AChR) loss in EAMG or are attracted to the NMJ secondary to tissue damage. In lethally irradiated young susceptible rats infiltrating macrophages were absent from the NMJ. However, similar AChR losses were observed in irradiated and non-irradiated rats. These results suggest that macrophages do not contribute to acetylcholine receptor loss in the effector phase of passive transfer EAMG and that age related resistance to passive transfer EAMG is not primarily determined by the absence of infiltrating macrophages.