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Open Access

7.1 Transgenic overexpression of CREM alpha in murine T cells results in an anergic phenotype with enhanced IL17 production

  • RL Lippe1,
  • KS Sturm1,
  • JR Roth1 and
  • KT Tenbrock2
Pediatric Rheumatology20086(Suppl 1):S11

Published: 15 September 2008


Systemic Lupus ErythematosusTransgenic MouseDermatitisTranscriptional RepressorContact Dermatitis

Background and methods

The cAMP responsive element modulator CREMa is a transcriptional repressor and putatively important in T cell pathophysiology of Systemic Lupus Erythematosus (SLE). To clarify the relevance of CREMa we overexpressed CREMa under control of the T cell specific CD2 promoter in mice.


As expected, overall T cell proliferation in naive T cells as response to different stimuli like anti-CD3 or an allogenic MLR was diminished in CREMa transgenic mice compared to wildtype mice, however-unexpectedly – disease activity in a contact dermatitis model was more severe in transgenic mice. Moreover, when T cells purified from the lymphnodes of the challenged ears were used for proliferation assays, transgenic T cell showed an enhanced proliferative response. Additionally, T cells from transgenic mice displayed an enhanced IL-17 production.


These data suggest that murine T cells with a transgenic overexpression of CREMa show an anergic phenotype in vitro, however when challenged in an in vivo disease model they react in a way, which predisposes to autoimmunity. Thus these T cells partially mimic the phenotype of human SLE T cells and support the relevance of CREMa for the pathophysiology of SLE.

Authors’ Affiliations

Inst of Immunology and Dept of Pediatrics, University of Muenster, Germany
Div of Pediatric Allergology and Immunology, Dept of Pediatrics, University of Aachen, Germany


© Lippe et al; licensee BioMed Central Ltd. 2008

This article is published under license to BioMed Central Ltd.