Publications by authors named "O Kessler"

Background: CD72 is a highly required regulatory molecule in B cells. Its sufficient expression is crucial for maintaining self-tolerance. In contrast, soluble CD72 (sCD72) is reported to be increased in the serum of autoimmune diseases such as systemic lupus erythematosus and primary Sjogren's syndrome (pSS).

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Introduction: Traumatic lumbar disc herniation (TLDH) without fracture in the motion segment is a rare occurrence compared with degenerative herniation.

Research Question: This study provides a systematic discussion of various aspects related to the diagnosis of TLDH.

Material And Methods: This review includes 12 cases of TLDH with MR-images since 2009 published in the PubMed and one adjunct illustration.

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Regulatory molecules have recently been recognized for their beneficial effects in the treatment of immune-mediated diseases, rather than using cytotoxic immune-suppressing drugs, which are associated with many unwanted side effects. Semaphorin3A (sema3A), a unique regulatory master of the immune system, was shown to be decreased in the serum of systemic lupus erythematosus (SLE) patients, in association with disease severity. Later, we were able to show its extremely beneficial effect in treating lupus nephritis in the NZB/W mice model.

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The semaphorin guidance factors receptor plexin-A2 transduces sema6A and sema6B signals and may mediate, along with plexin-A4, the anti-angiogenic effects of sema6A. When associated with neuropilins plexin-A2 also transduces the anti-angiogenic signals of sema3B. Here we show that inhibition of plexin-A2 expression in glioblastoma derived cells that express wild type p53 such as U87MG and A172 cells, or in primary human endothelial cells, strongly inhibits cell proliferation.

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CD72 is a regulatory co-receptor on B cells, with a role in the pathogenesis of systemic lupus erythematosus (SLE) in both human and animal models. Semaphorin3A (sema3A) is a secreted member of the semaphorin family that can reconstruct B cells' regulatory functions by upregulating IL-10 expression and inhibiting the pro-inflammatory activity of B and T cells in autoimmune diseases. The aim of our present study was to identify a new ligand for CD72, namely sema3A, and exploring the signal transduction pathways following its ligation in B cells.

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