Loss of autoimmune T cells correlates with brain diseases: possible implications for schizophrenia?
T-cell-mediated autoimmunity participates in physiological defense, maintenance and repair of the adult brain. However, unless such autoimmune responses to insults are rigorously controlled, they might lead to an autoimmune disease or other immune-related defects, where destructive activity outweighs the beneficial effect. Here, we discuss these apparently contradictory effects of autoimmunity in schizophrenic patients, whose typical immune aberrations have prompted recent speculation about an autoimmune-related etiology. We found that, although schizophrenic patients have active immune systems, they often lack autoimmune clones specifically reactive to a major myelin protein, myelin basic protein (MBP). This, in conjunction with our discovery in rodents that T cells that recognize brain-resident proteins are needed for normal cognitive functioning, led us to propose an immune-based neurodevelopmental hypothesis, in which autoimmune-T-cell deficiency is suggested to cause onset or progression of schizophrenia.
Department of Neurobiology, The Weizmann Institute of Science, 76100 Rehovot, Israel. jkipnis@unmc.edu
Jonathan
J
Kipnis
Michal
M
Cardon
Rael D
RD
Strous
Michal
M
Schwartz
D000293:Adolescent; D000328:Adult; D000818:Animals; D015551:Autoimmunity; D006801:Humans; D051379:Mice; D004676:Myelin Basic Protein / Q000276:immunology; D012559:Schizophrenia / Q000209:etiology / Q000276:immunology* / Q000503:physiopathology; D013601:T-Lymphocytes / Q000276:immunology*
D004676:Myelin Basic Protein