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Significant frequency deviation of the class I polymorphism HLA-A10 in schizophrenic patients
  1. B Laumbacher1,
  2. N Müller2,
  3. B Bondy2,
  4. B Schlesinger1,
  5. S Gu1,
  6. B Fellerhoff1,
  7. R Wank1
  1. 1From the Institute of Immunology, University of Muenchen, Germany
  2. 2Psychiatric Hospital, University of Muenchen, Germany
  1. Correspondence to:
 Dr R Wank, Institute of Immunology, University of Muenchen, Goethestrasse 31, 80336 Muenchen, Germany;
 wank{at}ifi.med.uni-muenchen.de

http://dx.doi.org/10.1136/jmg.40.3.217

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    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 region by linkage analysis.8–11 The HLA region spans 4000 kb and contains more than 100 genes. The peculiarity of this region is the high degree of polymorphism of most loci, that is, these loci encode a multitude of alleles which have evolved to fight a multitude of microbial factors.

    We analysed frequency deviations of HLA polymorphisms in two panels of patients with schizophrenia, collected at different times. HLA-A and HLA-C antigens were defined serologically in the patient and in random controls . HLA-C alleles were identified in addition by sequence based typing (SBT) using previously designed primers in the random controls and in patient panel 2.12 Genetic typing of HLA-C was indicated because of a generally poor expression of HLA-C antigens and therefore difficult serological assessment. Furthermore, higher resolution of HLA-C by sequencing did not show any stronger association with …

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