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Chapter 8 : Regulation of Antimicrobial Immunity
Authors:
Yasmine Belkaid1,
Sharvan Sehrawat2,
Barry T. Rouse3
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Affiliations:
1: Mucosal Immunology Unit, Laboratory of Parasitic Diseases, Division of Intramural Research, National Institute of Health, 4 Center Drive Bl-28, Bethesda, MD 20892;
2: Department of Pathobiology, College of Veterinary Medicine, University of Tennessee, 1414 Cumberland Ave., Knoxville, TN 37996;
3: Department of Pathobiology, College of Veterinary Medicine, University of Tennessee, 1414 Cumberland Ave., Knoxville, TN 37996
Content Type: Monograph
Publication Year:
2011
Category: Immunology; Clinical Microbiology
Book DOI:
10.1128/9781555816872
Chapter DOI:
10.1128/9781555816872.ch8
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Abstract:
This chapter focuses on inducible Foxp3+ T regulatory cells (Tregs). This cell type plays a dominant role in contributing to the maintenance of homeostasis and in limiting collateral tissue damage caused by chronic effector cell responses to pathogens. Microbial infections could trigger the expansion and activation of natural Treg (nTreg) in several ways, some of which may not involve engagement of the nTreg specific T-cell receptors (TCR), although this latter event might facilitate responses. Only a few reports have focused on Treg during acute infections and some have concluded that regulatory cells have little influence on the outcome. Even when Treg successfully preserve homeostasis in the host by controlling excessive immune responses, one consequence of such control is enhanced pathogen survival and, in some cases, long-term pathogen persistence are provided in the chapter. Some pathogens may cause Tr1 induction by producing a homolog of IL-10, but these are chronic infectious agents and are discussed in the chapter. Although hepatitis C virus (HCV) infection does expand the Treg population, no compelling evidence shows that the extent of one or more types of Treg responses correlates with the eventual outcome of infection. Importantly, Treg purified from the lymph node of human immunodeficiency virus (HIV) patients maintain their suppressive capacity against antiviral responses. The authors have evaluated whether or not manipulating Treg activity represents a useful way to modulate immunoinflammatory lesions caused by ocular infection with HSV.
Citation:
Belkaid Y, Sehrawat S, Rouse B.
2011.
Regulation of Antimicrobial Immunity,
p 109-120.
In
Kaufmann S, Rouse B, Sacks D (ed),
The Immune Response to Infection.
ASM Press, Washington, DC.
doi: 10.1128/9781555816872.ch8
Figures
Regulation of Antimicrobial Immunity
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Citation:
Belkaid Y, Sehrawat S, Rouse B.
2011.
Regulation of Antimicrobial Immunity,
p 109-120.
In
Kaufmann S, Rouse B, Sacks D (ed),
The Immune Response to Infection.
ASM Press, Washington, DC.
doi: 10.1128/9781555816872.ch8
/content/10.1128/9781555816872.ch08.ch08fig01
FIGURE 1
Microbes or their products may modulate Treg responses in multiple ways. A few Treg with TCR specificity to pathogen antigens proliferate in response to the infection. Alternatively, cross-reactive pathogen antigens or self-antigens, released as a result of tissue damaging inflammatory reactions, could stimulate self-reactive Treg. Stimulation independent of TCR could be provided by the microbial products such as TLR ligands or other host-derived products, such as cytokines (TGF-β, IL-2, IFN-γ, TNF-α, etc.), galectins (galectin-1, 9, and 10), heat shock proteins (Hsp-60, Hsp-60 peptide p277, Hsp-gp96, etc.), cellular metabolites (retinoic acid) as a result of infection.
10.1128/9781555816872/f0111-01_thmb.gif
10.1128/9781555816872/f0111-01.gif
FIGURE 1
Microbes or their products may modulate Treg responses in multiple ways. A few Treg with TCR specificity to pathogen antigens proliferate in response to the infection. Alternatively, cross-reactive pathogen antigens or self-antigens, released as a result of tissue damaging inflammatory reactions, could stimulate self-reactive Treg. Stimulation independent of TCR could be provided by the microbial products such as TLR ligands or other host-derived products, such as cytokines (TGF-β, IL-2, IFN-γ, TNF-α, etc.), galectins (galectin-1, 9, and 10), heat shock proteins (Hsp-60, Hsp-60 peptide p277, Hsp-gp96, etc.), cellular metabolites (retinoic acid) as a result of infection.
Citation:
Belkaid Y, Sehrawat S, Rouse B.
2011.
Regulation of Antimicrobial Immunity,
p 109-120.
In
Kaufmann S, Rouse B, Sacks D (ed),
The Immune Response to Infection.
ASM Press, Washington, DC.
doi: 10.1128/9781555816872.ch8
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Tables
Regulation of Antimicrobial Immunity
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Citation:
Belkaid Y, Sehrawat S, Rouse B.
2011.
Regulation of Antimicrobial Immunity,
p 109-120.
In
Kaufmann S, Rouse B, Sacks D (ed),
The Immune Response to Infection.
ASM Press, Washington, DC.
doi: 10.1128/9781555816872.ch8
/content/10.1128/9781555816872.ch08.ch08tab01
TABLE 1
Tregs in chronic infection
TABLE 1
Tregs in chronic infection
Citation:
Belkaid Y, Sehrawat S, Rouse B.
2011.
Regulation of Antimicrobial Immunity,
p 109-120.
In
Kaufmann S, Rouse B, Sacks D (ed),
The Immune Response to Infection.
ASM Press, Washington, DC.
doi: 10.1128/9781555816872.ch8
/content/10.1128/9781555816872.ch08.ch08tab02
TABLE 2
Strategies to boost Treg responses
TABLE 2
Strategies to boost Treg responses
Citation:
Belkaid Y, Sehrawat S, Rouse B.
2011.
Regulation of Antimicrobial Immunity,
p 109-120.
In
Kaufmann S, Rouse B, Sacks D (ed),
The Immune Response to Infection.
ASM Press, Washington, DC.
doi: 10.1128/9781555816872.ch8