Advances in Immunology [Vol 102] (AP, 2009) WW.pdf

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CONTRIBUTORS

Numbers in parentheses indicate the pages on which the authors’ contributions begin.

Eugene Agapov

Department of Medicine, Washington University School of Medicine,

St. Louis, Missouri, USA ( 245 )

John T. Battaile

Department of Medicine, Washington University School of Medicine,

St. Louis, Missouri, USA ( 245 )

Loralyn A. Benoit

Department of Medicine, Washington University School of Medicine,

St. Louis, Missouri, USA ( 245 )

Michael B. Brenner

Division of Rheumatology, Immunology and Allergy, Department of

Medicine, Brigham and Women’s Hospital, Harvard Medical School,

Boston, Massachusetts, USA ( 1 )

Derek E. Byers

Department of Medicine, Washington University School of Medicine,

St. Louis, Missouri, USA ( 245 )

Leonard Chess

Department of Medicine, College of Physicians and Surgeons, Columbia

University, New York, USA ( 95 )

Nadia R. Cohen

Harvard Division of Medical Sciences, Graduate Program in Immunol-

ogy, Boston, Massachusetts, USA ( 1 )

Salil Garg

Harvard Division of Medical Sciences, Graduate Program in Immunology

and Harvard-MIT MD PhD Program, Boston, Massachusetts, USA ( 1 )

Raif S. Geha

Division of Immunology, Children’s Hospital and Department of

Pediatrics, Harvard Medical School, Boston, Massachusetts, USA ( 135 )

vii

viii

Contributors

Mitchell H. Grayson

Department of Medicine, Washington University School of Medicine,

St. Louis, Missouri, USA ( 245 )

Rui He

Division of Immunology, Children’s Hospital and Department of

Pediatrics, Harvard Medical School, Boston, Massachusetts, USA ( 135 )

Michael J. Holtzman

Department of Cell Biology; and Department of Medicine, Washington

University School of Medicine, St. Louis, Missouri, USA ( 245 )

Hong Jiang

Department of Medicine, College of Physicians and Surgeons, Columbia

University, New York, USA; and Institute of Immunology, School of

Medicine, Shanghai Jiaotong University, Shanghai, PR China ( 95 )

Edy Y. Kim

Department of Medicine, Washington University School of Medicine,

St. Louis, Missouri, USA ( 245 )

Lalit Kumar

Division of Immunology, Children’s Hospital and Department of

Pediatrics, Harvard Medical School, Boston, Massachusetts, USA ( 135 )

Judy Lieberman

Immune Disease Institute and Department of Pediatrics, Harvard

Medical School, Boston, Massachusetts, USA ( 227 )

Michiko K. Oyoshi

Division of Immunology, Children’s Hospital and Department of

Pediatrics, Harvard Medical School, Boston, Massachusetts, USA ( 135 )

Chaeho Park

Department of Medicine, Washington University School of Medicine,

St. Louis, Missouri, USA ( 245 )

Anand C. Patel

Department of Pediatrics, Washington University School of Medicine,

St. Louis, Missouri, USA ( 245 )

Fabio Petrocca

Immune Disease Institute and Department of Pediatrics, Harvard

Medical School, Boston, Massachusetts, USA ( 227 )

Juhan Yoon

Division of Immunology, Children’s Hospital and Department of

Pediatrics, Harvard Medical School, Boston, Massachusetts, USA ( 135 )

Yingjian You

Department of Medicine, Washington University School of Medicine,

St. Louis, Missouri, USA ( 245 )

CHAPTER 1

Antigen Presentation by CD1:

Lipids, T Cells, and NKT Cells

in Microbial Immunity

Nadia R. Cohen, * , 1 Salil Garg, † , 1

and Michael B. Brenner ‡

Contents

Introduction

2. The CD1 Antigen Presentation Pathway: Chemistry,

Structure, and Cell Biology

2.1. Lipid antigens: Diversity and structure

2.2. CD1 structure: The binding and presentation

of microbial lipids

2.3. Antigen acquisition and uptake

2.4. The intersection of CD1 molecules and lipid

antigens: Trafficking

2.5. Antigen processing and loading

3. Group I CD1: CD1a, b, and c Molecules and T Cells

3.1. Expression of CD1 on DC and other

professional APC

3.2. TCRs of CD1a, b, and c-restricted T cells

3.3. Effector functions of CD1a, b, and c-restricted

T cells

3.4. Immune evasion of Group I CD1-based antigen

presentation

3.5. CD1a, b, and c responses in vivo and

vaccine potential

* Harvard Division of Medical Sciences, Graduate Program in Immunology, Boston, Massachusetts, USA

{ Harvard Division of Medical Sciences, Graduate Program in Immunology and Harvard-MIT MD PhD

Program, Boston, Massachusetts, USA

{ Division of Rheumatology, Immunology and Allergy, Department of Medicine, Brigham and Women’s

Hospital, Harvard Medical School, Boston, Massachusetts, USA

1 These authors equally contributed to this work

Advances in Immunology, Volume 102

# 2009 Elsevier Inc.

ISSN 0065-2776, DOI: 10.1016/S0065-2776(09)01201-2

Nadia R. Cohen et al.

4. Group II CD1: CD1d-Restricted T Cells: Activation,

Function, and Role in Antimicrobial Immunity

4.1. Activation of iNKT cells

4.2. The CD1d-restricted T cell immune response to

infection: Deployment, effector functions and

regulation

5. Role of CD1d-Restricted NKT Cells in Specific

Microbial Infections

5.1. CD1d-restricted T cells in immunity to bacteria

5.2. CD1d-restricted T cells in immunity to parasites

5.3. CD1d-restricted T cells in immunity to viruses

5.4. CD1d-restricted T cells in immunity to fungi

5.5. Evasion of CD1d-restricted T cell recognition

6. Conclusions

Acknowledgments

References

Abstract

The discovery of molecules capable of presenting lipid antigens,

the CD1 family, and of the T cells that recognize them, has opened a

new dimensionin our understanding of cell-mediated immunity

against infection. Like MHC Class I molecules, CD1 isoforms (CD1a,

b, c and d) are assembled in the ER and sent to the cell surface.

However, in contrast to MHC molecules, CD1 complexes are then

re-internalized into specific endocytic compartments where they

can bind lipid antigens. These include a broad scope of both self

and foreign molecules that range from simple fatty acids or phos-

pholipids, to more complex glycolipids, isoprenoids, mycolates and

lipopeptides. Lipid-loaded CD1 molecules are then delivered to the

cell surface and can be surveyed by CD1-restricted T cells expressing

ab or gd T Cell Receptors (TCR). It has become clear that T cell-

mediated lipid antigen recognition plays an important role in

detection and clearance of pathogens. CD1a, b and c-restricted

T cells have been found to recognize a number of lipid antigens

from M. tuberculosis. CD1d-restricted T cells are the only CD1-

restricted T cell subset present in mice, which lack the genes encod-

ing CD1a, b and c. Evidence from experiments in CD1d-restricted

T cell-deficient mice indicates that these cells play an important

role in the immune response against awide range of pathogens

including several bacteria, viruses and parasites. One subset of

CD1d-restricted T cells in particular, invariant Natural Killer T (iNKT)

cells, has been extensively studied. iNKT cells are characterized by

the expression of a semi-invariant TCR composed of a strictly con-

served a chain paired with a limited repertoire of b chains. During

infection, iNKT cells are rapidly elicited. Activated iNKT cells can

produce a vast array of cytokines that profoundly affect both the

innate and the adaptive arms of the immune response. In this review,

we describe the pathways and mechanisms of lipid antigen binding

and presentation by CD1 in detail, as well as the diverse roles played

by CD1-restricted T cells in the context of microbial infection.

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