Immune Recognition And Evasion Molecular Aspects Of Host Parasite Interaction

Immune Recognition and Evasion: Molecular Aspects of Host-Parasite Interaction reviews recent advances in understanding the genetic basis of host-parasite interactions, with emphasis on antigenic epitopes, the genetics of parasites, the molecular mechanisms of immune recognition and evasion, and the way that cytokines and hormones act on host-parasite interactions. Organized into four parts encompassing 25 chapters, this volume begins with an overview of the genomic organization of the T cell receptor genes and the contribution of non-B DNA structures to switch recombination in immunoglobulin genes. It then discusses signal transduction by class II molecules encoded by the major histocompatibility complex la and the biological consequences of this process; allelic polymorphism of HLA class II antigens and its connection to the molecular basis of autoimmunity; mimicry between HLAB27 and bacteria; and genetic control of susceptibility to helminth infection. The reader is also introduced to recognition of protein antigens by antibodies; recognition of influenza antigens by class I-restricted cytotoxic T lymphocytes; the biochemical basis of cachexia of infection; mechanisms of antigenic variation in Plasmodium; and rational design of trypanocidal drugs. Geneticists and molecular biologists will gain valuable information from this book.

The Janeway's Immunobiology CD-ROM, Immunobiology Interactive, is included with each book, and can be purchased separately. It contains animations and videos with voiceover narration, as well as the figures from the text for presentation purposes.

A very early step in microbial colonization and pathogenesis is that involving recog nition of the host by the microbe. In the final analysis such recognition is due to interaction between specific molecules on the two sides, without which host and microbe would ignore each other. It is therefore exciting to learn the rules that govern host-microbe interaction at to a large extent determines whether or not we are infected by the molecular level, which influenza virus, leishmanias, staphylococci and other pathogens. This book is a compendium of the addresses delivered at a symposium on molecular interaction at Porvoo, Finland in August 1991. Realizing that there are no a priori differ ences in receptor recognition in viruses, eukaryotic parasites and bacteria, we freely inter mingled these microbes at the symposium, and in this book. We found the interdisciplinary discussions and comparisons both educative and stimulating. Thus the book is divided into parts that focus on host cell receptors, on microbial recognition molecules and molecules that mediate microbial interaction with a host cell receptor and, briefly, on the molecular events that follow. Although many microbes and many cellular receptors are missing from the book -owing to the limited duration and size of the symposium -the articles presented here constitute an impressive body of examples of how initial host-microbe interaction can come about. We believe that as such the book is a useful and interesting overview of the mechanisms and principles involved in these interactions.

Multiple demographic or economic parameters contribute to the origin of emerging infections, for example: poverty, urbanization, climate change, conflicts and population migrations. All these factors are a challenge to assess the impact (present and future) of parasitic diseases on public health. The intestine is a major target of these infections; it is a nutrient-rich environment harbouring a complex and dynamic population of 100 trillion microbes: the microbiome. Most researches on the microbiome focus on bacteria, which share the gut ecosystem with a population of uni- and multi cellular eukaryotic organisms that may prey on them. Our interest focuses on the families of eukaryotic microbes inhabiting the intestine, called “intestinal eukaryome”, that include fungi, protists and helminths. Knowledge on the reciprocal influence between the microbiome and the eukaryome, and on their combined impact on homeostasis and intestinal diseases is scanty and can be considered as an important emerging field. Furthermore, the factors that differentiate pathogenic eukaryotes from commensals are still unknown. This book presents an overview of the science presented and discussed in the First Eukaryome Congress held from October 16th to 18th, 2019 at the Pasteur Institute in Paris. This book covers the following topics: Phylogenetic, prevalence, and diversity of intestinal eukaryotic microbes; and their (still enigmatic) historical evolution and potential contributions to mucosal immune homeostasis. Integrative biology to study the molecular cell biology of parasite-host interactions and the multiple parameters underlining the infectious process. The exploitation of tissue engineering and microfluidics to establish three-dimensional (3D) systems that help to understand homeostasis and pathological processes in the human intestine.

Parasites cause many important diseases in humans and domestic animals, malaria being an example. Parasites have evolved to exploit hosts' bodies whereas hosts have evolved immune systems to control infections. Host-parasite interactions therefore provide fascinating examples of evolutionary 'arms-races' in which the immune system plays a key role. Modern research in immunoparasitology is directed towards understanding and exploiting the capacity to develop effective anti-parasite immunity. By concentrating on selected infections where research has made significant progress, Immunity to Parasites provides a clear account of how host immune responses operate and how parasites can evade immunity. The experimental basis of this research is emphasised throughout. This completely updated second edition includes an expanded section on anti-parasite vaccines. The text is aimed at undergraduates and postgraduates with interests in either parasitology or immunology and provides introductory sections on these topics to lead the reader into the later chapters.

The biological bases of invertebrate immune responses have interested scientists for decades, from the first relevant observation by E. Metchnikoff in 1882, who discovered phagocytosis while studying starfish larvae. Invertebrate immunology first began to be appre ciated as an important field in the late 1960s and 1970s. However, in the following years there was much controversy regarding the question: do invertebrates offer insight into the origin of the sophisticated immune responses of the vertebrates? There are several reasons why progress in research on invertebrate immune competence has been painfully slow. One of the main impediments to the progress, as compared to the fast development of knowledge in the vertebrate systems, was the fact that most of the studies concentrated on "whole organism" assays, mainly on grafting tissues between allogeneic partners. Only in the last few years have more and more aspects of invertebrate immunity been investigated on the cellular, biochemical and molecular levels. These studies led to discoveries of novel defense reactions, new pathways of effector mechanisms which are elicited after recognition of "nonself', and complex, sometimes highly polymorphic genetic elements that control invertebrate immune reactions. The importance of invertebrate immunity for understanding "immunology" as a whole, despite the conflicting models and hypotheses, is now much more recognized than before. Although most of the 20 phyla belonging to the inver tebrates have different modes of life, body organizations, habitats occupied, and biochemical patterns, they show striking aspects of exceptional precision for discriminating between self and nonself.

The ability of pathogens, such as parasites, bacteria, fungi and viruses to invade, persist and adapt in both invertebrate and vertebrate hosts is multifactorial and depends on both pathogen and host fitness. Communication between a pathogen and its host relies on a wide and dynamic array of molecular interactions. Through this constant communication most pathogens evolved to be relatively benign, whereas killing of its host by a pathogen represents a failure to adapt. Pathogens are lethal to their host when their interaction has not been long enough for adaptation. Evolution has selected conserved immune receptors that recognize signature patterns of pathogens as non-self elements and initiate host innate responses aimed at eradicating infection. Conversely, pathogens evolved mechanisms to evade immune recognition and subvert cytokine secretion in order to survive, replicate and cause disease. The cell signaling machinery is a critical component of the immune system that relays information from the receptors to the nucleus where transcription of key immune genes is activated. Host cells have developed signal transduction systems to maintain homeostasis with pathogens. Most cellular processes and cell signaling pathways are tightly regulated by protein phosphorylation in which protein kinases are key protagonists. Pathogens have developed multiple mechanisms to subvert important signal transduction pathways such as the mitogen activated protein kinase (MAPK) and the nuclear factor kB (NF-kB) pathways. Pathogens also secrete effectors that manipulate actin cytoskeleton and its regulators, hijack cell cycle machinery and alter vesicular trafficking. This research topic focuses on the cellular signaling mechanisms that are essential for host immunity and their subversion by pathogens.