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Biomedical subjects

H U Scherer

Publications and source records attributed to H U Scherer.

7 recordsLinked to original sources
PubMed2006

[Polyarteritis nodosa - a "classical" case].

Diagnosis of polyarteritis nodosa is often delayed due to the vast heterogeneity of initial clinical symptoms. The case presented shows the clinical image of the disease, leading from the first symptoms up to verification of the diagnosis by sural-nerve biopsy. We discuss the classification of the disease among other types of vasculitis, the classification criteria proposed by the American College of Rheumatology (ACR) as well as current therapeutic options. This case underlines the interdisciplinary character of the disease, challenging neurologists, dermatologists, rheumatologists and orthopedics alike.

Amines↗
PubMed2005

[Rheumatology].

The advent of monoclonal antibodies for the treatment of rheumatic diseases has revolutionized our understanding of therapeutic efficacy. Only a few years ago, response rates of >70% combined with significant reductions in inflammatory activity and radiologic progression would have been impossible. At the same time, however, issues of safety and cost have gained in importance and challenge physicians and patients alike. Making these new drugs available to as many eligible patients as possible requires a thorough documentation of disease activity using standardized outcome measures as well as a profound knowledge of their safety profiles. In addition, institutional guidelines for the use of these agents need to be as close to the cutting edge of science as possible. The following article presents an overview of currently available biologic agents in rheumatology and a prospect of those to come.

Animals↗
PubMed2000

The heat shock protein gp96 induces maturation of dendritic cells and down-regulation of its receptor.

Peptides associated with the heat shock protein gp96 induce a specific T cell response against cells from which gp96 is isolated. Recently, we have shown that gp96 binds to a yet unknown receptor present on dendritic cells (DC) and that receptor-mediated uptake is required for cross-presentation of gp96-associated peptides by DC. We now describe that gp96 mediates maturation of DC as determined by up-regulation of MHC class II and CD86 molecules, secretion of the cytokines IL-12 and TNF-alpha and enhanced T cell stimulatory capacity. Heat-denatured gp96 is not able to induce DC maturation and cytokine secretion. Furthermore, we show that mature DC are no longer able to bind gp96 molecules. Hence, the gp96 receptor is down-regulated on mature DC, suggesting that this receptor behaves similar to other receptors involved in antigen uptake like the scavenger receptor CD36, the mannose receptor or the integrins alpha(v)beta(3) and alpha(v)beta(5). Together, our findings provide an additional explanation for the remarkable immunogenicity of gp96 as a cross-priming antigen carrier and direct activator of DC.

Animals↗
PubMed2000

The heat shock protein gp96: a receptor-targeted cross-priming carrier and activator of dendritic cells.

Heat shock proteins like gp96 (grp94) are able to induce specific cytotoxic T-cell (CTL) responses against cells from which they originate and are currently studied in clinical trials for use in immunotherapy of tumors. We have recently demonstrated that gp96 binds to at least one yet unidentified receptor restricted to antigen-presenting cells (APCs) like dendritic cells (DCs) but not to T cells. Moreover we have shown, that for CTL activation by gp96-chaperoned peptides receptor-mediated uptake of gp96 by APCs is required. Lately, we have discovered a second function of gp96 when interacting with professional APCs. Gp96 is able to mediate maturation of DCs as determined by upregulation of MHC class II, CD86 and CD83 molecules, secretion of pro-inflammatory cytokines IL-12 and TNF-alpha and enhanced T-cell simulatory capacity. Furthermore, the gp96 receptor(s) are down-regulated on mature DCs, suggesting that the gp96 receptor(s) behave similar to other endocytic receptors like CD36, mannose receptor etc. Our findings now provide additional evidence for the remarkable immunogenicity of gp96: first, the existence of specific gp96 receptors on APCs and second, the capacity to activate dendritic cells which is strictly required to enable these highly sophisticated APCs to prime CTL responses.

Animals↗