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  • 1
    Keywords: RECEPTOR ; CELLS ; ENDOTHELIAL-CELLS ; EXPRESSION ; PROTECTION ; CELL ; Germany ; MODEL ; MODELS ; NF-KAPPA-B ; ACTIVATION ; CELL ACTIVATION ; MECHANISM ; TRANSCRIPTION FACTOR ; mechanisms ; DELETION ; STEPS ; SIGNALING PATHWAYS ; PRODUCT ; SUPERFAMILY ; innate immunity ; Jun ; SOLUBLE RECEPTOR ; immune response ; IMMUNE-RESPONSE ; RECEPTORS ; INITIATION ; inflammation ; ANIMAL-MODELS ; immunoglobulin ; PRODUCTS ; LEADS ; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS ; pattern recognition ; CLASS-III REGION ; DIABETIC VASCULOPATHY ; INFLAMMATORY RESPONSES
    Abstract: While the initiation of the adaptive and innate immune response is well understood, less is known about cellular mechanisms propagating inflammation. The receptor for advanced glycation end products (RAGE), a transmembrane receptor of the immunoglobulin superfamily, leads to perpetuated cell activation. Using novel animal models with defective or tissue-specific RAGE expression, we show that in these animal models RAGE does not play a role in the adaptive immune response. However, deletion of RAGE provides protection from the lethal effects of septic shock caused by cecal ligation and puncture. Such protection is reversed by reconstitution of RAGE in endothelial and hematopoietic cells. These results indicate that the innate immune response is controlled by pattern-recognition receptors not only at the initiating steps but also at the phase of perpetuation
    Type of Publication: Journal article published
    PubMed ID: 15173891
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  • 2
    Keywords: PEPTIDE ; CELLS ; IN-VITRO ; CELL ; COMBINATION ; Germany ; VITRO ; SYSTEM ; MICE ; TIME ; ACTIVATION ; MECHANISM ; MARKER ; INDUCTION ; animals ; ANTIGEN ; DENDRITIC CELLS ; mechanisms ; T cell ; T cells ; T-CELL ; T-CELLS ; TOLERANCE ; MOLECULE ; DELETION ; NERVOUS-SYSTEM ; TRANSGENIC MICE ; PROGRESSION ; NUMBER ; MARKERS ; CENTRAL-NERVOUS-SYSTEM ; MULTIPLE-SCLEROSIS ; T lymphocytes ; AUTOIMMUNE ENCEPHALOMYELITIS ; AUTOIMMUNITY ; thymus ; THYMIC EPITHELIAL-CELLS ; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS ; MS ; multiple sclerosis ; immunology ; regulatory T cells ; animal ; nervous system ; central nervous system ; ANTIGEN RECOGNITION ; AUTOREACTIVE T-CELLS ; BASIC-PROTEIN GENE ; CD4(+) T cell ; RECEPTOR-ALPHA CHAINS ; TOLERANCE INDUCTION
    Abstract: Most autoantigens implicated in multiple sclerosis (MS) are expressed not only in the central nervous system (CNS) but also in the thymus and the periphery. Nevertheless, these autoantigens might induce a strong autoimmune response leading to severe destruction within the CNS. To investigate the influence of a dominantly presented autoantigen on experimental autoimmune encephalomyelitis (EAE), we generated transgenic mice expressing the autoantigenic peptide MBP1-10 covalently bound to the MHC class II molecule I-A(u). These mice were crossed either with B10.PL or with TCR-transgenic Tg4 mice, specific for the transgenic peptide-MHC combination. In double transgenic mice we found strong thymic deletion and residual peripheral T cells were refractory to antigen stimulation in vitro. Residual peripheral CD4(+) T cells expressed activation markers and a high proportion was CD25 positive. Transfer of both CD25-negative and CD25-positive CD4(+) T cells from double transgenic animals into B10.PL mice strongly inhibited the progression of EAE. Despite this thorough tolerance induction, some double transgenic mice developed severe signs of EAE after an extended period of time. Our data show that in the circumstances where autoantigenic priming persists, and where the number of antigen-specific T cells is high enough, autoimmunity may prevail over very potent tolerance-inducing mechanisms
    Type of Publication: Journal article published
    PubMed ID: 16361316
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