Umfang:
Online-Ressource (X, 178p. 21 illus., 20 illus. in color, digital)
Ausgabe:
1
ISBN:
9781461404842
,
9781283353083
Serie:
SpringerLink
Inhalt:
The interface between host and pathogen cells involves a complex series of molecular mechanisms. On one side host cells recognize pathogen structures and initiate immune responses. On the other side, pathogens continually evolve immune escape strategies aiming at establishing chronic disease and transmission to a new host. The balance between those two forces can determine the fate of infectious diseases. Either uncontrolled pathogen replication or tissue damage due to unleashed pro-inflammatory responses can be detrimental to the host. Here we explore immune regulatory mechanisms that take place during some of the most relevant infectious diseases worldwide. We provide a wide spectrum view of the current understanding of how the immune system modulates ongoing responses to prevent host pathology, as well as some immune evasion strategies used by some of those microbes
Inhalt:
Upon infection, the host needs to mount vigorous immune response against pathogen in order to successfully control its replication. However, once the infectious agent is controlled or eliminated, host cells need to signal the immune system to slow or cease its activities. While vast knowledge has been accumulated through the years on the mechanisms involved in the initiation and effector phases of the immune responses, the pathways triggered in order to modulate or end innate and acquired immunity are becoming more evident as evidence for its relevance comes to surface. Due to its biological p
Anmerkung:
Includes bibliographical references and index
,
Control of Innate and Adaptive Immune Responses during Infectious Diseases; Preface; Contents; Contributors; Chapter 1: Resolution of Inflammation During Toxoplasma gondii Infection; 1.1 Introduction; 1.2 Experimental T. gondii Infection; 1.2.1 Microbial Recognition and IL-12 Induction; 1.2.2 IFN-?, Th1 Cells and Microbicidal Activity; 1.3 Pro-resolution Strategies as a Mechanism to Prevent Immunopathology; 1.3.1 Resolution Phase of the Inflammatory Response; 1.3.2 Interleukin-10; 1.3.3 TGF-ß; 1.3.4 IL-22; 1.3.5 IL-27; 1.3.6 Lipoxin A 4; 1.3.7 Redundancy and Control of Inflammation
,
1.3.8 Induction of Endogenous LXA 4 as an Pathogen Evasion Pathway1.4 Conclusions; References; Chapter 2: Mechanisms of Host Protection and Pathogen Evasion of Immune Response During Tuberculosis; 2.1 Introduction; 2.2 Infection and Innate Immunity; 2.2.1 Neutrophils; 2.2.2 T Cells; 2.2.3 Dendritic Cells; 2.2.4 Natural Killer Cells; 2.2.5 Regulatory T Cells; 2.3 Granuloma Formation and Containment of Bacilli; 2.3.1 TNF; 2.3.2 IFN-?; 2.3.3 Lipoxins; 2.3.4 IL-10; 2.3.5 TGF-ß; 2.4 Evasion of Immune Response; 2.4.1 Cell Wall Components; 2.4.2 Inhibition of Phagolysosome Fusion
,
2.4.3 Mycobacterial Dormancy2.4.4 Modulation of Host Cell Signaling; 2.5 Disease Reactivation; 2.6 Vaccines, Chemotherapy in the Interface with the Immune System; References; Chapter 3: NKT Cell Activation During (Microbial) Infection; 3.1 Introduction; 3.2 NKT Cells and the CD1 System; 3.2.1 Group I CD1 Molecules Recognizing NKT Cells (CD1a, b, c); 3.2.2 Group II CD1 Molecules Recognizing iNKT Cells (CD1d); 3.2.2.1 CD1d: Restricted Invariant NKT Cells (iNKT Cells, Type I NKT Cells); 3.2.2.2 CD1d-Restricted Diverse NKT Cells (Type II NKT Cells, Non-classical NKT Cells)
,
3.2.3 Group III CD1 Molecules (CD1e)3.2.4 Species Distribution of CD1 Molecules; 3.3 iNKT Cell Function; 3.4 CD1d Mediated Presentation of Gsls; 3.5 Self-GSL Antigens for CD1d Molecules; 3.6 Activation of iNKT Cells During Bacterial Infection; 3.6.1 Indirect, Bystander Activation of iNKT Cells by Gram-Negative, LPS-Positive Bacteria; 3.6.2 Direct, Cognate Recognition of GSL Antigens in the Cell Wall of Gram-Negative LPS-Negative Alphaproteobacteria; 3.7 Activation of iNKT Cells During Non-bacterial Infection; 3.7.1 Viral Infections; 3.7.2 Parasitic, Helminth and Fungal Infections
,
3.8 Human Studies3.8.1 Correlation of iNKT Cell Numbers with Susceptibility to Infection; 3.8.2 Infections with Novosphingobium/Sphingomonas Spp. in Clinical Settings; 3.8.3 Association of Primary Biliary Cirrhosis with Novosphingobium Aromaticivorans; 3.8.3.1 Role of GSL Recognition from Novosphingobium spp . by iNKT Cells in the Pathogenesis of Primary Biliary Cirrhosis (PBC); 3.8.3.2 Pathogenesis of Primary Biliary Cirrhosis (PBC); 3.8.3.3 Specific Recognition of PDC-E2 Homologues in Novosphingobium aromaticivorans by Sera of PBC Patients
,
3.9 Mouse Model of Infection-Induced Primary Biliary Cirrhosis
Weitere Ausg.:
ISBN 9781461404835
Weitere Ausg.:
Buchausg. u.d.T. ISBN 9781461404835
Sprache:
Englisch
Fachgebiete:
Medizin
Schlagwort(e):
Infektionskrankheit
;
Immunreaktion
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