Loss of autoimmune T cells correlates with brain diseases: Possible implications for schizophrenia?

Jonathan Kipnis, Michal Cardon, Rael D. Strous, Michal Schwartz

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish
Pages (from-to)107-112
Number of pages6
JournalTrends in Molecular Medicine
Volume12
Issue number3
DOIs
StatePublished - Mar 2006

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