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
3
1.
Introduction
2. The CD1 Antigen Presentation Pathway: Chemistry,
Structure, and Cell Biology
3
2.1. Lipid antigens: Diversity and structure
3
2.2. CD1 structure: The binding and presentation
of microbial lipids
9
2.3. Antigen acquisition and uptake
16
2.4. The intersection of CD1 molecules and lipid
antigens: Trafficking
19
24
2.5. Antigen processing and loading
28
3. Group I CD1: CD1a, b, and c Molecules and T Cells
3.1. Expression of CD1 on DC and other
professional APC
28
30
3.2. TCRs of CD1a, b, and c-restricted T cells
3.3. Effector functions of CD1a, b, and c-restricted
T cells
31
3.4. Immune evasion of Group I CD1-based antigen
presentation
33
3.5. CD1a, b, and c responses in vivo and
vaccine potential
34
*
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
All rights reserved.
1
2
Nadia R. Cohen et al.
4. Group II CD1: CD1d-Restricted T Cells: Activation,
Function, and Role in Antimicrobial Immunity
35
35
4.1. Activation of iNKT cells
4.2. The CD1d-restricted T cell immune response to
infection: Deployment, effector functions and
regulation
40
5. Role of CD1d-Restricted NKT Cells in Specific
Microbial Infections
49
5.1. CD1d-restricted T cells in immunity to bacteria
50
5.2. CD1d-restricted T cells in immunity to parasites
59
5.3. CD1d-restricted T cells in immunity to viruses
63
5.4. CD1d-restricted T cells in immunity to fungi
66
5.5. Evasion of CD1d-restricted T cell recognition
66
68
6. Conclusions
Acknowledgments
70
References
70
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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