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Dendritic Cell Biology as an Immune Dysfunction in Neoplasia

Autor Lawrence M. Agius
en Limba Engleză Paperback – 27 feb 2022
This monograph deals with the susceptibility issues in the development of an effective response to antigenicity as presented by emerging or established neoplastic lesions. An attempt has been made to present critical views of the dysfunction of carcinogenesis in terms of evolving immune responses in terms of recruitment of dendritic cell biology. It is within such conceptual framework that autoimmunity presents an attractive response to neoplasia in terms that allow for access to the malignant transformation process. It is significant to potentiate the immune responses that involve the integral immune dimensions that characterize and recharacterize the dynamics of turnover of dendritic cells as the most powerful agents in presentation of neoantigenicity as provided by tumor cell proliferation and spread within the body. The performance of staged dimensions in antigen exposure by tumor cells is critical to the presentation of tumor cells as brought forward by the proposed dynamics of an interface between tumor cells and the tumor microenvironment in the realization of an extensive autoimmune response with the realization of performance exposure of the antigenicity as a biologic agent in its own right. This book is aimed to cancer researchers, pathologists, and immunologists with a strong interest in carcinogenesis and cancer cell progression as dictated by proposed immune response to tumor antigenicity.
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Specificații

ISBN-13: 9781685074869
ISBN-10: 1685074863
Pagini: 198
Dimensiuni: 152 x 229 mm
Greutate: 0.3 kg
Editura: Nova Science Publishers Inc
Colecția Nova Science Publishers Inc

Cuprins

Preface; Active Participation of Dendritic Cells in Tumor Cell Immune Evasion; Aging-Induced Aberrant Dendritic Cells in Terms of Highly Proliferative Tumor Cell Clonal Subsets; Sustained Metabolic System Imbalance as Induced Immune Suppression of Dendritic Cells in Tumor Neoantigenicity Profiles; Inclusive Loss of Integrity of The Antitumor Immune Response as Chemokine Patterns of Nonrecognition; Incongruent Biology of Redistributed Chemokine Action in Carcinogenesis; The Nature of Modulated Redistribution of Integral Immunity as System Redefinition of Clinical Non-Responsiveness to the Antitumor Antigenicity; Complexity of Inter-Activities of Suppressed Immune Response with Dendritic Cell Development and Differentiation in Tumors; System Profiles of Dendritic Cell Motility as Modeled Tumor Cell Proliferation and Spread; Duality of Unstable Dynamics of Emerging Tumor Cells and of Infiltrating Dendritic Cells in Carcinogenesis; Systems of Predetermination of Cytokine/Chemokine Action Towards Cancer Antigenicity in Terms of Dendritic Cell Plasticity; Exosome System Preferences as Integral to the Immune Response and Immune Non-Response to Tumor Neoantigens; Constitution of a Failed Antitumor Immune Response as Carcinogenesis Sustainment; Multiple Models of Failed Immune Responses Redefine Carcinogenesis; Effect Dominance of Integral Cytokine/Chemokine Networks in Tumor Cell Antigenicity Response; Incongruent Dislocation of Epitope Spread as Immunosuppression Dynamics of Tumor Cell Clones; Systems of Immune Evasion are Inherent to the Inflammatory Response to Tumorigenesis; Heterogeneous Dendritic Cell Subset Interchange as Tumor Immunosuppression; Recurrent Immune Responses Are Primary Reactivity to the Tumor Microenvironment Rather Than to the Integral Tumor Cells Themselves; The Immunologic Non-Response is a Physiologic, Conditional and Homeostatic State of an Integral Immune System Towards Tumor Antigenicity; Dendritic Cell Plasticity as History of Performance Dynamics; Contact Mechanics of Immune Evasion Involve Suppression of The Antigen-Presentation Step and of the Tumor-Mirrored Migration of the Dendritic Cells; Microenvironmental Reproducible Immunomodulation as Proposed Growth and Spread of Malignant Cells in Terms of Neoantigenicity; Tumor Cell Necrosis Modulates the Immune Tolerance Induced by the Tumor Microenvironment; Index.