Immunotherapy Research Center E.V

München, Germany

Immunotherapy Research Center E.V

München, Germany
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Wank R.,Immunotherapy Research Center E.V | Laumbacher B.,Immunotherapy Research Center E.V | Fellerhoff B.,Ludwig Maximilians University of Munich
Future Neurology | Year: 2013

Chlamydia has attracted increased attention as a possible cause of atheromatous plaques, cerebrovascular diseases, multiple sclerosis, Alzheimer's disease and schizophrenia. The Chlamydia species are obligate intracellular parasites. The unique biphasic life cycle of Chlamydia permits the parasite to persist in cells for years. Acute Chlamydia infections can be recognized serologically in the peripheral blood through observation of rising antibody titers or molecularly using various PCR methods. However, the identification of chronic Chlamydia infection is hampered by many hurdles. This has initiated controversial discussions about the true involvement of Chlamydia, particularly in the CNS. The aspects of the discussion will be inspected as well as the vulnerability of the neuronal MHC to immune reactions. © 2013 Future Medicine Ltd.


Gu S.,Immunotherapy Research Center e.V. | Fellerhoff B.,Immunotherapy Research Center e.V. | Fellerhoff B.,Ludwig Maximilians University of Munich | Muller N.,Ludwig Maximilians University of Munich | And 2 more authors.
Immunobiology | Year: 2013

Neuronal MHC/HLA regulates the synapses of the central nervous system (CNS). The expression of MHC/HLA is, in turn, regulated by immune cytokines. We were therefore interested in the regulation of schizophrenia-associated HLA antigens, specifically their regulation of expression by interferons. We had previously observed a moderately increased frequency of HLA-A10 expression in schizophrenic patients. While searching for the "true" disease gene near the HLA-A gene, we discovered that homozygosity of the HLA-J M80469 pseudogene allele, in combination with HLA-A10 or HLA-A9, was associated with a high risk of schizophrenia (HLA-A10 relative risk = 29.33, p= 0.00019, patients N= 77, controls N= 214). The allele HLA-J M80468, which codes for interferon-inducible mRNA, conferred protection on carriers of HLA-A9 and HLA-A10 (HLA-A10 relative risk = 0.022, p= 0.00017). Functional analysis revealed that interferon γ (IFNγ) downregulated the expression of HLA-A9 and HLA-A10 in monocytes from HLA-J M80469 homozygous patients but not from carriers of the HLA-J M80468 allele. This is the first demonstration of an inverse effect of IFNγ on HLA expression that is associated with non-coding gene variants and schizophrenia. Our findings suggest that the interferons secreted during acute and chronic infections may interfere in synaptic regulation via neuronal HLA and that this disturbance in synaptic regulation may induce the symptoms of mental illness. © 2012.


PubMed | Immunotherapy Research Center e.V.
Type: Journal Article | Journal: Immunobiology | Year: 2013

Neuronal MHC/HLA regulates the synapses of the central nervous system (CNS). The expression of MHC/HLA is, in turn, regulated by immune cytokines. We were therefore interested in the regulation of schizophrenia-associated HLA antigens, specifically their regulation of expression by interferons. We had previously observed a moderately increased frequency of HLA-A10 expression in schizophrenic patients. While searching for the true disease gene near the HLA-A gene, we discovered that homozygosity of the HLA-J M80469 pseudogene allele, in combination with HLA-A10 or HLA-A9, was associated with a high risk of schizophrenia (HLA-A10 relative risk = 29.33, p = 0.00019, patients N = 77, controls N = 214). The allele HLA-J M80468, which codes for interferon-inducible mRNA, conferred protection on carriers of HLA-A9 and HLA-A10 (HLA-A10 relative risk = 0.022, p = 0.00017). Functional analysis revealed that interferon (IFN) downregulated the expression of HLA-A9 and HLA-A10 in monocytes from HLA-J M80469 homozygous patients but not from carriers of the HLA-J M80468 allele. This is the first demonstration of an inverse effect of IFN on HLA expression that is associated with non-coding gene variants and schizophrenia. Our findings suggest that the interferons secreted during acute and chronic infections may interfere in synaptic regulation via neuronal HLA and that this disturbance in synaptic regulation may induce the symptoms of mental illness.

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