TY - JOUR
T1 - Loss of autoimmune T cells correlates with brain diseases
T2 - Possible implications for schizophrenia?
AU - Kipnis, Jonathan
AU - Cardon, Michal
AU - Strous, Rael D.
AU - Schwartz, Michal
N1 - Funding Information:
We thank S.R. Smith for editing the manuscript. M.S. holds the Maurice and Ilse Katz Professorial Chair in Neuroimmunology. The work was supported by Proneuron Ltd, Industrial Park, Ness-Ziona, Israel (M.S.), and by Nebraska Tobacco Settlement Biomedical Research Development Fund (NTSBRDF)(J.K.).
PY - 2006/3
Y1 - 2006/3
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=33644990839&partnerID=8YFLogxK
U2 - 10.1016/j.molmed.2006.01.003
DO - 10.1016/j.molmed.2006.01.003
M3 - Article
C2 - 16469540
AN - SCOPUS:33644990839
SN - 1471-4914
VL - 12
SP - 107
EP - 112
JO - Trends in Molecular Medicine
JF - Trends in Molecular Medicine
IS - 3
ER -