© 2003 BMJ Publishing Group
LETTER TO JMG
Significant frequency deviation of the class I polymorphism HLA-A10 in schizophrenic patients
1 From the Institute of Immunology, University of Muenchen, Germany
2 Psychiatric Hospital, University of Muenchen, Germany
Correspondence to:
Correspondence to:
Dr R Wank, Institute of Immunology, University of Muenchen, Goethestrasse 31, 80336 Muenchen, Germany;
wank@ifi.med.uni-muenchen.de
Keywords: HLA class I polymorphism; schizophrenia; HLA immunogenetics
| The first 150 words of the full text of this article appear below. |
The central nervous system (CNS) and the immune system communicate bidirectionally.1,2 Immune cell subpopulations produce neurotrophins like neurotrophin-3 (NT-3), brain derived neurotrophic factor (BDNF), and dopamine.3,4 Such subpopulations are vulnerable to infection and may impair feedback loops to neuronal cells as chronically infected carriers. Successful elimination of infection depends mainly on successful presentation of microbial antigens by HLA molecules, that is, on inherited HLA alleles. The recognition of a major contribution of genetic factors to the aetiology of schizophrenia marks one of the highlights in the research into schizophrenia. Foster parents of schizophrenics do not induce the disease in adopted children from healthy parents and healthy foster parents cannot prevent the development of schizophrenia in children from schizophrenic parents.5 Different chromosomes have been pinpointed as harbouring genes involved in the pathogenesis of schizophrenia.6,7 Several researchers have found evidence for schizophrenia vulnerability genes on chromosome 6p close to the HLA genetic
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