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Increased Toll-Like Receptor (TLR) 2 and TLR4 Expression in Monocytes from Patients with Type 1 Diabetes: Further Evidence of a Proinflammatory State.

Increased Toll-Like Receptor (TLR) 2 and TLR4 Expression in Monocytes from Patients with Type 1 Diabetes: Further Evidence of a Proinflammatory State. Research Abstract Details 

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  • Increased Toll-Like Receptor (TLR) 2 and TLR4 Expression in Monocytes from Patients with Type 1 Diabetes: Further Evidence of a Proinflammatory State. Abstract Text:

    sridevi devarajSridevi Devaraj,mohan r dasuMohan R Dasu,jason rockwoodJason Rockwood,william winterWilliam Winter,steven c griffenSteven C Griffen,ishwarlal jialalIshwarlal Jialal,

    Context: Type 1 diabetes (T1DM) is associated with increased cardiovascular mortality. It is a pro-inflammatory state as evidenced by increased circulating biomarkers and monocyte activity. The toll-like receptors (TLRs) are pattern recognition receptors, expressed abundantly on monocytes. TLR2 and TLR4 are important in atherosclerosis. However, there is a paucity of data examining TLR2 and TLR4 expression in T1DM and examining its contribution to the proinflammatory state. Objective: Thus, we examined TLR2 and TLR4 expression in monocytes from T1DM patients compared with controls (n = 31 per group). Setting: The study was performed at the University of California Davis Medical Center. Patients: Healthy controls (n = 31) and T1DM patients (n = 31) were included in the study. Results: TLR2 and TLR4 surface expression and mRNA were significantly increased in T1DM monocytes compared with controls. Downstream targets of TLR, nuclear factor kappaB, myeloid differentiation factor 88, Trif, and phosphorylated IL-1 receptor-associated kinase were significantly up-regulated in T1DM. Finally, the release of IL-1beta and TNF-alpha was significantly increased in monocytes from T1DM compared with controls and correlated with TLR2 and TLR4 expression (P < 0.005). In addition, TLR2 and TLR4 expression was significantly correlated to glycosylated hemoglobin, carboxymethyllysine, and nuclear factor kappaB (P < 0.02). Conclusion: Thus, we make the novel observation that TLR2 and TLR4 expression and signaling are increased in T1DM and contribute to the proinflammatory state.

    Increased Toll-Like Receptor (TLR) 2 and TLR4 Expression in Monocytes from Patients with Type 1 Diabetes: Further Evidence of a Proinflammatory State. Publishing Authors By Initials

    s devarajS Devaraj,mr dasuMR Dasu,j rockwoodJ Rockwood,w winterW Winter,sc griffenSC Griffen,i jialalI Jialal,

    For similar abstracts research abstracts see: abstracts research

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    Increased Toll-Like Receptor (TLR) 2 and TLR4 Expression in Monocytes from Patients with Type 1 Diabetes: Further Evidence of a Proinflammatory State. Journal Published:

    PUBLICATION TYPE: Journal Article

    Journal: The Journal of clinical endocrinology and metaboli

    VOLUME: 93

    Page Numbers: 578-83

    Journal Abbreviation: J. Clin. Endocrinol. Metab.

    ISSN: 0021-972X

    DAY: 20

    MONTH: 11

    YEAR: 2007

    Increased Toll-Like Receptor (TLR) 2 and TLR4 Expression in Monocytes from Patients with Type 1 Diabetes: Further Evidence of a Proinflammatory State. Information

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    LANGUAGE: eng

    NlmUniqueID: 375362

    Increased Toll-Like Receptor (TLR) 2 and TLR4 Expression in Monocytes from Patients with Type 1 Diabetes: Further Evidence of a Proinflammatory State. Keywords Mesh Terms:

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    Grant and Affiliation Information for Increased Toll-Like Receptor (TLR) 2 and TLR4 Expression in Monocytes from Patients with Type 1 Diabetes: Further Evidence of a Proinflammatory State.

    AFFILIATION: Laboratory for Atherosclerosis and Metabolic Research, University of California Davis Medical Center, 4635 II Avenue, Research I Building, Room 3000, Sacramento, California 95817. ijialal@ucdavis.edu.

    Country: United States

    United States Research PublicationUnited States Research Publication

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    MEDLINETA: J Clin Endocrinol Metab

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