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Immunoglobulin-deficient rats fail to develop experimental allergic encephalomyelitis.
Journal of Neuroimmunology
|October 1, 1983
Summary
Newborn rats treated to lack B-cells and antibodies did not develop experimental autoimmune encephalomyelitis (EAE). This suggests B-cell antibody production is essential for EAE induction.
Area of Science:
- Immunology
- Neuroscience
Background:
- Experimental autoimmune encephalomyelitis (EAE) is an animal model for multiple sclerosis.
- The role of B-cells and antibodies in EAE pathogenesis is not fully understood.
Purpose of the Study:
- To investigate the necessity of B-cell function for EAE induction in Lewis rats.
Main Methods:
- Neonatal rats were treated with rabbit anti-rat IgM antiserum to induce B-cell deficiency.
- Adult rats were sensitized with spinal cord homogenate or myelin basic protein (BP).
- Immune responses (antibody production, T-cell function) and EAE development were assessed.
Main Results:
- B-cell deficient rats showed no detectable serum IgM and reduced IgG levels.
- These rats failed to produce antibodies to sheep red blood cells (SRBC) or BP.
- B-cell deficient rats did not develop clinical or histological signs of EAE.
- T-cell functions, such as response to PHA and tissue allograft rejection, remained intact.
Conclusions:
- B-cell immunoglobulin and antibody production are critical for the induction of experimental autoimmune encephalomyelitis (EAE).
- T-cell mediated immunity is not sufficient for EAE development in the absence of B-cell function.