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   <subfield code="a">Recognition of self-heat shock protein 60 by T cells from patients with atopic dermatitis</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Berber Kapitein, Joost Aalberse, Mark Klein, Wilco de Jager, Maarten Hoekstra, Edward Knol, Berent Prakken]</subfield>
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   <subfield code="a">Heat shock protein 60 (hsp60) is a highly conserved stress protein and target of self-reactive T cells in various inflammatory diseases. Not much is known about a possible role in atopic disease. As atopic diseases are considered to be the result of a disturbance in the balance between T helper cells type 2 and regulatory T cells, it is of interest to know whether hsp60 acts as a bystander antigen in atopic disease. Our aim was to investigate whether hsp60 is involved in the chronicity of inflammation of atopic dermatitis (AD). We studied the expression of hsp60 in skin tissue of adults with AD by immunohistochemistry. Peripheral blood mononuclear cells (PBMC) of children with AD were cultured with hsp60 and proliferative responses, cytokine secretion, surface markers, and functional assays were compared to responses of PBMC of healthy controls (HC). Hsp60 was detected more in lesional skin of AD patients compared to nonlesional skin. Furthermore, PBMC of children with AD proliferated more strongly in response to hsp60 compared to HC. hsp60-reactive T cells of atopic children produced high levels of IFNγ and low levels of IL-10. In vitro activation with hsp60 leads to the induction of CD4+CD25bright T cells expressing FOXP3 in both HC as well as in atopic children. However, despite their regulatory phenotype, hsp60-induced CD4+CD25brightCD127−FOXP3+ T cells of AD patients were incapable of suppressing effector T cells in vitro. hsp60 is recognized by proinflammatory (IFNγ high, IL-10 low) T cells in atopic patients and is more present in lesional AD skin. This suggests that hsp60-specific T cell responses contribute to local inflammation in AD.</subfield>
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   <subfield code="a">Cell Stress Society International, 2012</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Atopy</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Atopic dermatitis</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Regulatory T cells</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Human heat shock protein 60</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">TH2 : T helper cells type 2</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">TH1 : T helper cells type 1</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Tregs : Naturally occurring or induced CD4+CD25+FOXP3+ regulatory T cells</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">hsp : Heat shock protein(s)</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">hsp60 : Human heat shock protein 60</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">PBMC : Peripheral blood mononuclear cells</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">AD : Atopic dermatitis</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">FACS : Fluorescence-activated cell sorting</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Kapitein</subfield>
   <subfield code="D">Berber</subfield>
   <subfield code="u">Department of General Paediatrics, Wilhelmina Children's Hospital, Utrecht, Netherlands</subfield>
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   <subfield code="a">Aalberse</subfield>
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   <subfield code="u">Department of General Paediatrics, Wilhelmina Children's Hospital, Utrecht, Netherlands</subfield>
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   <subfield code="a">Klein</subfield>
   <subfield code="D">Mark</subfield>
   <subfield code="u">Department of Paediatric Immunology, University Medical Centre Utrecht, Wilhelmina Children's Hospital, KC 01.069.0, P.O. Box 85090, 3508 AB, Utrecht, Netherlands</subfield>
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   <subfield code="a">de Jager</subfield>
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   <subfield code="u">Department of Paediatric Immunology, University Medical Centre Utrecht, Wilhelmina Children's Hospital, KC 01.069.0, P.O. Box 85090, 3508 AB, Utrecht, Netherlands</subfield>
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   <subfield code="a">Hoekstra</subfield>
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   <subfield code="u">Department of General Paediatrics, Wilhelmina Children's Hospital, Utrecht, Netherlands</subfield>
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   <subfield code="a">Knol</subfield>
   <subfield code="D">Edward</subfield>
   <subfield code="u">Department of Dermatology, University Medical Centre Utrecht, Utrecht, The Netherlands</subfield>
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   <subfield code="a">Prakken</subfield>
   <subfield code="D">Berent</subfield>
   <subfield code="u">Department of Paediatric Immunology, University Medical Centre Utrecht, Wilhelmina Children's Hospital, KC 01.069.0, P.O. Box 85090, 3508 AB, Utrecht, Netherlands</subfield>
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   <subfield code="t">Cell Stress and Chaperones</subfield>
   <subfield code="d">Springer Netherlands</subfield>
   <subfield code="g">18/1(2013-01-01), 87-95</subfield>
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   <subfield code="u">Department of Paediatric Immunology, University Medical Centre Utrecht, Wilhelmina Children's Hospital, KC 01.069.0, P.O. Box 85090, 3508 AB, Utrecht, Netherlands</subfield>
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