Decoding The Genomic Control Of Immune Reactions
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Decoding the Genomic Control of Immune Reactions
This book explores existing and potential strategies for using the genome sequences of human, mouse, other vertebrates and human pathogens to solve key problems in the treatment of immunological diseases and chronic infections. The assembled genome sequences now provide important opportunities for solving these problems, but a major bottleneck is the identification of key sequences and circuits controlling the relevant immune reactions. This will require innovative, interdisciplinary and collaborative strategies of a scale and complexity we are only now beginning to comprehend. Specific problems addressed include the following: What kinds of information are we lacking to understand how the genome sequence specifies the differentiation and response of immune system cells, and system behaviour such as immunological memory and tolerance? Which genome sequences and cellular circuits cause or prevent pathological immune responses to foreign pathogens, allergens or self-tissues? Which host and pathogen genome sequences and cellular circuits explain the failure of sterilizing immune responses to sophisticated human pathogens such as the agents of tuberculosis, malaria, metazoan parasites and chronic viruses? Containing contributions from a range of leading experts in the field, this book provides an important new perspective for clinical immunologists and basic researchers alike.
Models and Estimation of Genetic Effects
Author: José M Álvarez-Castro
language: en
Publisher: Frontiers Media SA
Release Date: 2015-04-17
Ronald Fisher needed to develop elaborate models of genetic effects in order to set the foundations of Quantitative Genetics in his 1918 paper “The correlation between relatives on the supposition of Mendelian inheritance”. Since then, many significant implementations have been made to model genetic effects. However, at the verge of one century after Fisher’s kick-off, models of genetic effects keep on being discussed and implemented. Indeed, the relatively recent advent of QTL analyses challenged the state of the art of this field by providing researchers the opportunity to obtain and analyze estimates of genetic effects from real data. In this context, the development of this field was not exempt of some polemics, like the debate about the convenience of the functional and the statistical epistasis approaches. This research topic is meant to provide recent developments in models and estimation of genetic effects and to enrich the discussion about how and why models of genetic effects must be further developed and applied. The articles in this Research Topic shall thus extend, refine and/or provide a refresh look at Fisher’s original models of genetic effects and their application to genetic effects estimation and to improve our understanding of evolutionary processes and breeding programs.
Genetic and Epigenetic Control on Immune Responses Regulating Molecules in Cancer Development, Progression, and Treatment
Author: Katherine Chiappinelli
language: en
Publisher: Frontiers Media SA
Release Date: 2024-10-16
In line with recent evidence, the development of cancer has been described as uncontrolled cell growth that results from gradual accumulation of genetic and epigenetic alterations, involving aberrations in oncogenes, tumor suppressor genes, and defects in genes engaged in DNA repair. As a result, cancer cells acquire a neoplastic phenotype and tumor-associated antigens (TAAs) are presented on their surface. These target structures should be recognized by cells of the immune system. However, a sequence of events at the genetic and epigenetic level disturb immune cells, and in consequence, make them unable to eliminate cancer cells. Both innate and adaptive immunity are mobilized against cancer cells. In response to the appearance of cells with malignant transformation, NK cells release perforin and granzyme, causing direct cytolysis of the target cells. They can also secrete pro-inflammatory cytokines and in that way enhance the anticancer response. The activity of NK cells is regulated by a variety of activating and inhibitory receptors including NKG2D, KIR, CD94 -NKG2 heterodimers and natural cytotoxicity receptors, TNF family ligands, as well as co-stimulatory receptors, which recognize related molecules on target cells. A fundamental trigger of the anticancer immune response is the recognition of TAAs by T cells, via the major histocompatibility complex (MHC), which should be followed by signals from co-stimulatory molecules. Full activation of T lymphocytes requires a third signal provided by the presence of cytokines, and this leads to cell proliferation, differentiation, and secretion of chemokines and cytokines. The effect is to drive the clonal expansion of the T cells directed against TAAs and to recruit other immune effector cells in order to enhance immune defense.