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34 - Pathogens and Inflammation

from PART VI - ANIMAL MODELS OF INFLAMMATION

Published online by Cambridge University Press:  05 April 2014

By
Julio Aliberti
Edited by
Charles N. Serhan ,
Peter A. Ward  and
Derek W. Gilroy
With contributions by
Samir S. Ayoub
Julio Aliberti
Affiliation:
University of Cincinnati College of Medicine
Charles N. Serhan
Affiliation:
Harvard Medical School
Peter A. Ward
Affiliation:
University of Michigan, Ann Arbor
Derek W. Gilroy
Affiliation:
University College London
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Summary

Here, we discuss the modulation of inflammation upon pathogen invasion, including the new pathway triggered by lipoxin involved in the repression of immune response during infection, as well as this mechanism from the perspective of the pathogen, which pirates the host's lipoxygenase machinery to its own advantage as a probable immune-escape mechanism.

INNATE IMMUNITY AND PATHOGENS

It is well known that a series of pattern-recognition receptors is involved in the recognition of different microbial pathogens and induction of the innate response. Such receptors recognize distinct biochemical patterns of molecules displayed by the invading pathogen. The repertoire of innate immune receptors is very broad and includes several classes of germ-line–encoded proteins such as Toll-like receptors (TLRs), scavenger receptors, and C-type lectins. This wide array of recognition molecules allows the host to detect a variety of microbial molecules including carbohydrates, lipids, nucleic acids, and proteins [1, 2]. Distinct TLR ligands provide distinct activation status and cytokine production patterns for antigen-presenting cells (APCs), resulting in the induction of differential immune responses. Thus, TLRs are critical molecules to induce not only inflammatory responses but also fine-tune adaptive immune responses depending on invading pathogens [3]. TLRs activation can upregulate costimulatory molecules on APC, thus enhancing the activation of adaptive T-cell responses.

Type
Chapter
Information
Fundamentals of Inflammation , pp. 448 - 456
Publisher: Cambridge University Press
Print publication year: 2010

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