Publications by authors named "I Bartok"

Microscopic studies performed on extracted human teeth after their preparation in advance is helpful in a relatively good reestablishment of the treatment steps that have been applied to these teeth, as well as an evaluation of the quality of such treatments. Therefore, we have used stereo- and optical microscopy, highlighting aspects of external morphology, as well as root canal space of an extracted mandibular second premolar, subjected to prosthetic and endodontic treatment. In order to verify some technical errors that might occur during the endodontic and restorative treatment, we tried to appreciate the quality of the root canal filling and cervical defect and access cavity restoration of an extracted premolar #45.

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Deficiency of C1q, the initiator of the complement classical pathway, is associated with the development of systemic lupus erythematosus (SLE). Explaining this association in terms of abnormalities in the classical pathway alone remains problematic because C3 deficiency does not predispose to SLE. Here, using a mouse model of SLE, we demonstrate that C1q, but not C3, restrains the response to self-antigens by modulating the mitochondrial metabolism of CD8 T cells, which can themselves propagate autoimmunity.

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αβ T cells respond to peptide epitopes presented by major histocompatibility complex (MHC) molecules. The role of T cell receptor (TCR) germline complementarity determining regions (CDR1 and 2) in MHC restriction is not well understood. Here, we examine T cell development, MHC restriction and antigen recognition where germline CDR loop structure has been modified by multiple glycine/alanine substitutions.

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The bias of αβ T cells for MHC ligands has been proposed to be intrinsic to the T-cell receptor (TCR). Equally, the CD4 and CD8 coreceptors contribute to ligand restriction by colocalizing Lck with the TCR when MHC ligands are engaged. To determine the importance of intrinsic ligand bias, the germ-line TCR complementarity determining regions were extensively diversified in vivo.

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T cell receptor transfer is an attractive strategy for the generation of antigen specific T cells to target infection and malignancy. Cross pairing of the transduced and endogenous TCR chains produces new and potentially auto-reactive specificities and dilutes the therapeutic TCR. This is further complicated as the efficiency of pairing for each alphabeta pair is unpredictable and the factors which influence it are not well characterized.

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