The Cytoskeleton in T Cell Migration and Activation PDF Download
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Author: Jerome Delon
Publisher: Frontiers Media SA
ISBN: 2832506259
Category : Medical
Languages : en
Pages : 140
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Book Description
Author: Jerome Delon
Publisher: Frontiers Media SA
ISBN: 2832506259
Category : Medical
Languages : en
Pages : 140
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Book Description
Author: Bruce Alberts
Publisher:
ISBN: 9780815332183
Category : Cytology
Languages : en
Pages : 0
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Book Description
Author: Irene Yin-Ting Chang
Publisher:
ISBN:
Category :
Languages : en
Pages : 184
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Book Description
T cells are required by their immunological roles to recirculate in the body and migrate to tissue sites, a journey that exposes them to distorting forces and physical obstacles that hinder their movement. Therefore, they must possess appropriate deformability to accommodate and adapt to these mechanical stimuli to migrate unimpeded. Since T cells alter their physical properties and migration routes upon activation, they may possess dissimilar mechanical properties as a result of this process. This hypothesis was tested using the techniques micropipette aspiration and atomic force microscopy, which allow the investigation of the elastic and viscous responses of single T cells. It was discovered that the activation process reduced T cell stiffness by more than three folds, a finding that agrees with the motility gain observed in activated T cells. The same testing procedure was applied to Wiskott-Aldrich syndrome protein (WASp)-deficient T cells that exhibit abnormal morphology and impaired chemotaxis. The stiffness of the diseased cells in the naive state was 1.5 times less than that of the non-diseased cells, a result that may be due to the disrupted polymerization and cross-linking of the actin cytoskeleton in the absence of WASp, a regulator of actin growth and organization. Furthermore, the viscous response of the diseased cells in the activated state was found to be impaired. Chemokines were found to dramatically reduce the stiffness of naive T cells that were induced to migrate. These findings suggest that WASp plays an important role in maintaining cell mechanical property and facilitating T cell extravasation by tailoring the cells' deformability. At the molecular level, activation of T cells is triggered by the binding of their surface receptors to antigens, a mechanism that is also key in T cell development. In both cases, the bond strength, conventionally measured by the affinity (KD) or the dissociation rate (koff) of the interacting pair, dictates the biological outcome. Since a few weak interactions may nudge a sub-threshold signal over the threshold strength, and observing that the current methods for measuring KD and koff lack the resolution to detect very weak bonds, this work explored the possibility of utilizing dynamic force spectroscopy (DFS) to study very weak binding strengths. Preliminary results confirm this capability.
Author: Jonathan Soboloff
Publisher: CRC Press
ISBN: 149870509X
Category : Medical
Languages : en
Pages : 258
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Book Description
T cells play a vital role mediating adaptive immunity, a specific acquired resistance to an infectious agent produced by the introduction of an antigen. There are a variety of T cell types with different functions. They are called T cells, because they are derived from the thymus gland. This volume discusses how T cells are regulated through the operation of signaling mechanisms. Topics covered include positive and negative selection, early events in T cell receptor engagement, and various T cell subsets.
Author: Amanda Lorene Martin
Publisher:
ISBN:
Category : Cellular control mechanisms
Languages : en
Pages : 256
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Book Description
Author: Huan Zheng (Ph.D.)
Publisher:
ISBN:
Category :
Languages : en
Pages : 130
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Book Description
The overarching theme of this thesis is to develop and apply multi-scale computational techniques adopted from physical sciences to study a key phenomenon underlying the adaptive immune response: the activation of T cells. The specific objectives are: 1) develop efficient and versatile computational frameworks to study multi-scale biological systems in silico; 2) obtain mechanistic insights into how T cells are triggered in vivo. The first problem investigated in this thesis addressed a controversy regarding when and how T cells alter migratory patterns in lymphoid tissues, as observed in intravital microscopy experiments. By developing a lattice-based model for T cell migration coupled with a mechanistically motivated simple scheme for T cell activation, I showed that the quantity and quality of cognate antigen (Ag) presented by dendritic cells (DC) dictate such changes. The results from theoretical and computational analyses were not only in agreement with synergistic experiments, but also made predictions that have been tested positively. Furthermore, I identified a consolidated measure of Ag quantity and quality, which provides a unifying conceptual framework for considering diverse future experimental results. The results from this study also suggested that T cells may integrate sub-optimal signals derived from successive encounters with DCs to achieve full activation. However, an underlying molecular mechanism that may confer such "short term memory" of exposure to Ag is not known. I explored the possibility that the hysteresis resulting from positive feedback regulation of the catalytic conversion of a G-protein RasGDP to RasGTP in the T cell receptor (TCR) membrane-proximal signaling network may enable such "short term memory". I developed a multiscale computational model that combines stochastic simulations of the TCR membrane-proximal signaling network with T cell migration. The results showed that this hysteresis can enable T cells to integrate signals derived from weakly stimulatory DCs and may greatly enhance the detection sensitivity during disease onset when Ag presentation is low. The computational framework developed in this study can be readily adapted to examine diverse biological systems where signaling and cell motion need to be studied simultaneously. For example, the model was modified to investigate a DC-mediated mechanism for signal integration, and our results suggest that this mechanism is less likely. Initial steps were also taken to construct a macroscopic model that aims to study how T cell activation impacts observations at the organismic level. Preliminary results for how microscopic receptor-ligand interactions affect the proliferation of different T cell types are presented. Directions for future research are suggested based on these findings.
Author: Jose C. Jimenez-Lopez
Publisher: BoD – Books on Demand
ISBN: 9535131699
Category : Science
Languages : en
Pages : 344
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Book Description
The cytoskeleton is a highly dynamic intracellular platform constituted by a three-dimensional network of proteins responsible for key cellular roles as structure and shape, cell growth and development, and offering to the cell with "motility" that being the ability of the entire cell to move and for material to be moved within the cell in a regulated fashion (vesicle trafficking). The present edition of Cytoskeleton provides new insights into the structure-functional features, dynamics, and cytoskeleton's relationship to diseases. The authors' contribution in this book will be of substantial importance to a wide audience such as clinicians, researches, educators, and students interested in getting updated knowledge about molecular basis of cytoskeleton, such as regulation of cell vital processes by actin-binding proteins as cell morphogenesis, motility, their implications in cell signaling, as well as strategies for clinical trial and alternative therapies based in multitargeting molecules to tackle diseases, that is, cancer.
Author:
Publisher: Academic Press
ISBN: 0128096217
Category : Science
Languages : en
Pages : 350
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Book Description
Piezo Channels, Volume 79, the latest volume in the Current Topics in Membranes series provides the necessary membrane research to assist readers in discovering the current state of a particular field and future directions. New chapters in the updated volume include A Tour de Force: The Discovery, Properties, and Function of Piezo Channels, Piezo1 Channels in Vascular Development and the Sensing of Shear Stress, the Origin of the Force: The Force-From-Lipids Principle Applied to Piezo Channels, Genetic Diseases of PIEZO1 and PIEZO2 Dysfunction, and The Structural Basis for Sensing by the Piezo1 Protein. Users of this series will find an up-to-date presentation of the current knowledge in the field of Piezo Channels. Written by leading experts in the field Contains original material, both textual and illustrative, that make it a very relevant reference Presented in a very comprehensive manner Ideal reference for both researchers in the field and general readers who will find this book to be relevant and up-to-date
Author: William Thomas Nels Simonson
Publisher:
ISBN:
Category :
Languages : en
Pages : 190
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Book Description
Author: Klaus Ley
Publisher: Frontiers Media SA
ISBN: 2889194302
Category : Chemokines
Languages : en
Pages : 109
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Book Description
Arrest chemokines are a small group of chemokines that promote leukocyte arrest from rolling by triggering rapid integrin activation. Arrest chemokines have been described for neutrophils, monocytes, eosinophils, naïve lymphocytes and effector memory T cells. Most arrest chemokines are immobilized on the endothelial surface by binding to heparin sulfate proteoglycans. Whether soluble chemokines can promote integrin activation and arrest is controversial (Alon-Gerszten). Many aspects of the signaling pathway from the GPCR chemokine receptor to integrin activation are the subject of active investigation. Leukocyte adhesion deficiency III is a human disease in which chemokine-triggered integrin activation is defective because of a mutation in the cytoskeletal protein kindlin-3. About 10 different such mutations have been described. The defects seen in patients with LAD-III elucidate the importance of rapid integrin activation for host defense in humans. We welcome reports that help clarifying this crucial first step in the process of leukocyte transendothelial migration.
