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"Our findings suggest that inhibiting or depleting B lymphocytes, the cells that produce antibodies, may promote healing and reduce the long-term effects of spinal cord injury," says study leader Phillip G. Popovich, professor of neuroscience and of molecular virology, immunology and medical genetics and director of the Center for Brain and Spinal Cord Repair.

"They may also help explain why the central nervous system does not repair itself efficiently and why other impairments often follow spinal cord injury."

To learn whether these antibodies could on their own damage the spinal cord, the investigators purified them from the blood of injured mice and microinjected them into one side of the spinal cord of uninjured normal mice.

Within 48 hours, the hind leg on the side of the injection site became paralyzed, and remained partially so after one week. The animals also showed loss of neurons and other damage to the spinal cord.

"This was one of the more striking, remarkable aspects of the study, the fact that the antibodies alone from an injured animal can activate an immune response that damages tissue in an uninjured animal," says Ankeny, a research scientist in molecular virology, immunology and medical genetics.

"These experiments essentially prove that the antibodies have the potential by themselves to make spinal lesions worse."

T effectors outfox T regulators in autoimmunity
Findings from a mouse model of multiple sclerosis suggest that regulatory T cells alone cannot outduel pathogenic T
cells in the central nervous system. The observations may have implications for experimental approaches designed to
dampen autoimmune diseases by infusion of regulatory T cells.

Abstract

The damage in ischemic stroke is caused by two events: (i) the ischemic phenomenon by itself; (ii) the self-destructive mechanisms developed as a consequence of ischemia. The inflammatory response is one of these destructive phenomena that accompanies and exacerbates the developing injury. Since it has been suggested that immune cells participate in neuroprotective and restorative processes, modulation rather than elimination of this inflammatory response could be a strategy to improve the neurological outcome. The immune modulator copolymer-1 (Cop-1), a synthetic basic random copolymer of amino acids, is a potent inducer of Th2 regulatory cells which, aside from exerting modulatory actions, is capable of releasing neurotrophic factors. There is evidence that Cop-1-specific T cells exert neuroprotective and even restorative effects in diverse neurodegenerative diseases. In order to test the ability of Cop-1 to prevent ischemic injury in a model of transient middle cerebral artery (MCA) occlusion, two groups of rats were treated either with Cop-1 or with saline solution (SS). Seven days after occlusion, Cop-1 treated rats presented a significant improvement in neurological function compared to SS-treated animals (1.2 ± 0.4 and 2.8 ± 0.5 mean ± S.D., respectively; p = 0.008). Histological findings showed that the percentage of infarct volume was smaller in Cop-1 treated rats (4.8 ± 1.5), in comparison with those receiving SS (32.2 ± 8.6; p = 0.004). Cop-1 constitutes a promising therapy for stroke; thereby, the enforcement of further experimental investigation is encouraged in order to be able to formulate the best strategy.

mrhodes40 wrote:I take cop too, it makes some pretty sore lumps but in 12 or so years of taking I have never had anything remotely bad in terms of reaction. It also controls me RA really well.........

sadly the stuff is off patent and they will not be testing it for RA or other inflammatory diseases.