ISSN:
1432-2196
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Conclusion The antibody detected in the ALS sera with suppressive activity for terminal sprouting is likely directed against an antigen that is normally sequestered. Tolerance to the 56 kd antigen described here is not exhibited in rats, as syngenic immunizations induce an immune response (M. E. Gurney, unpublished observation). Freshly denervated muscle secretes very low amounts of the 56 kd antigen, and the level of secretion rises 2–3 days after denervation in vivo. Of the few antecedent events associated with ALS by case studies, mechanical injuries, participation in physical activities, or bone fractures might all produce nerve damage or periods of limb immobilization [48]. Similar physical insults are stimuli for sprouting in animal models [13, 39], and might result in elevated secretion of sprouting factor, resulting in induction of an immune response in susceptible individuals. The antibodies detected in this study could arise as a secondary response to neuromuscular destruction, as occurs following tissue injury in many organs. The absence of inhibitory activity in sera of patients with neuropathy suggests that denervation per se need not give rise to development of such antibodies, although the extent of denervation and muscle atrophy in the ALS patients was, in general, markedly greater than in patients with neuropathy. Whether sprouting inhibitory antibodies prove to be of primary pathogenic significance, or are only a secondary phenomenon, they provide potentially significant reagents with which to elucidate the existence and nature of human motor neuron growth factors.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00197252
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