Advances in Immunology - Frederick W. Alt

Advances in Immunology

Frederick W. Alt (Redaktør)

Advances in Immunology, a long-established and highly respected publication, presents current developments as well as comprehensive reviews in immunology. Articles address the wide range of topics that comprise immunology, including molecular and cellular activation mechanisms, phylogeny and molecular evolution, and clinical modalities. Les mer
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Advances in Immunology, a long-established and highly respected publication, presents current developments as well as comprehensive reviews in immunology. Articles address the wide range of topics that comprise immunology, including molecular and cellular activation mechanisms, phylogeny and molecular evolution, and clinical modalities. Edited and authored by the foremost scientists in the field, each volume provides up-to-date information and directions for future research.
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Forlag: Academic Press Inc
Innbinding: Innbundet
Språk: Engelsk
ISBN: 9780123737090
Format: 23 x 15 cm
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Contributorsix
1. New Insights into Adaptive Immunity in Chronic Neuroinflammation1




Volker Siffrin, Alexander U. Brandt, Josephine Herz, and Frauke Zipp





1. Introduction: Multiple Sclerosis Is a Heterogeneous Inflammatory Disease of the Nervous System

2




2. Experimental Autoimmune Encephalomyelitis as a Model for MS

3




3. Current Knowledge About Induction and Perseveration of Chronic Neuroinflammation

5




3.1 General considerations

5




3.2. CD4+ T helper cells in chronic neuroinflammation

5




3.3. CD8+ T cells in neuroinflammation: A never-ending controversy

15




3.4. B cells and antibody-mediated immune responses in chronic neuroinflammation

17




4. Therapeutic Approaches to Chronic Neuroinflammation

20




4.1. General considerations

20




4.2. Current therapeutic concepts

21




4.3. New therapeutic concepts

23




References

29
2. Regulation of Interferon-γ During Innate and Adaptive Immune Responses41




Jamie R. Schoenborn and Christopher B. Wilson





1. Introduction

43




2. IFN-γ-Producing Cells

45




2.1. NK cells

45




2.2. NKT cells

45




2.3. CD8 T cells

46




2.4. CD4 T cells play multiple roles in adaptive immunity

46




3. Signaling Pathways Controlling IFN-γ Production by NK Cells

48




3.1. NK receptors provide a dynamic rheostat to control NK cell responses

48




3.2. IL-12 is a potent activator of IFN-γ production in NK cells

49




3.3. IL-15 and IL-2 regulate NK cell development and contribute to IFN-γ production

51




3.4. TGF-β is a negative regulator of IFN-γ production and NK cell development

51




4. Control of IFN-γ Production by NKT Cells

52




5. Signaling Pathways in the Differentiation of CD4 and CD8 T Cells

53




5.1. Naive T cells require antigen stimulation for proliferation and effector commitment

53




5.2. T cells require cytokine signals for sustained IFN-γ expression

54




5.3. Other factors influencing Th1 lineage commitment

57




5.4. TGF-β and IL-6 negatively regulate IFN-γ production and Th1 development

58




5.5. IFN-γ production by memory T cells in response to cytokine stimulation

59




6. Transcription Factors Downstream of the TCR, Activating NK Receptors, and Cytokine Receptors

60




6.1. Factors downstream of the TCR, costimulatory, and activating NK receptors

60




6.2. STATs are activated in response to cytokine receptor signaling

68




6.3. T-box family members are crucial for IFN-γ secretion

70




7. Epigenetic Processes Govern Plasticity of Cell Fate Choices and Help to Identify Distal Regulatory Elements

72




8. Transcriptional Regulatory Elements Within the Ifng Gene

74




8.1. Regulatory elements within the Ifng promoter and gene

74




8.2. Identification of candidate distal regulatory elements in the Ifng locus

77




9. Functional Analysis of Candidate Distal Regulatory Elements in the Ifng Locus

82




10. Conclusions and Future Directions

84




Acknowledgments

85




References

85
3. The Expansion and Maintenance of Antigen-Selected T Cell Clones103




Douglas T. Fearon





1. Background

105




1.1. Introduction

105




1.2. Subsets of antigen-selected CD8+ T cells: Central memory, effector memory, and effector cells

106




1.3. Central memory CD8+ T cells generate new effector CD8+ T cells

107




1.4. Current models for development of antigen-stimulated CD8+ T cells

108




2. The Behavior of the CD8+ T Cell in Persistent Viral Infections

111




2.1. Persistent CD8+ T cell stimulation and expansion: "Inflationary" epitopes

111




2.2. Cellular senescence despite continued clonal expansion

113




2.3. Clonal persistence versus clonal succession

114




2.4. Molecular requirements for clonal persistence

114




3. Clarifying the Role of IL-2 in the Clonal Expansion and Effector Differentiation of the CD8+ T Cell

115




3.1. Is IL-2 "the" or "a" mediator of CD8+ T cell clonal expansion?

115




3.2. CD8+ T cell clonal expansion without IL-2R signaling

116




4. Coreceptors Mediating IL-2-Independent CD8+ T Cell Clonal Expansion

118




4.1. CD27

118




4.2. Other coreceptors

120




5. Modifying the Antiproliferative Effects of Types I and II IFN

120




5.1. The effects of types I and II IFN on CD8± T cells

121




5.2. Regulating IFN-γR expression

121




5.3. Statl as a "Switch" determining the effects of types I and II IFN on proliferation

122




6. Transcriptional Control of Replicative Senescence: Bmi-1, Blimp-1, and BCL6/BCL6b

123




7. A Refined Model for CD8+ T Cell Clonal Expansion: Sequential Phases of CD27-Dependent Self-Renewal and IL-2-Dependent Differentiation

126




8. Clinical Extensions of the TCR/CD27 Pathway: Adoptive CD8+ T Cell Therapy

127




Acknowledgments

129




References

129
4. Inherited Complement Regulatory Protein Deficiency Predisposes to Human Disease in Acute Injury and Chronic Inflammatory States141




Anna Richards, David Kavanagh, and John P. Atkinson





1. Altered Self Triggers Innate Immunity

143




1.1. Acute injury

143




1.2. Debris accumulation

144




2. Regulation of the Alternative Complement Pathway

145




2.1. Overview of activation

145




2.2. Regulation of the alternative complement pathway

148




2.3. Regulatory proteins

148




3. Lessons from Homozygous Complement Regulatory Protein Deficiencies

153




3.1. Plasma proteins FH and Fl

153




3.2. Membrane proteins MCP and Crry

153




4. Complement and Atypical Hemolytic Uremic Syndrome

154




4.1. Hemolytic uremic syndrome

154




4.2. Factor H

155




4.3. FH-related genes

157




4.4. Membrane cofactor protein: CD46

157




4.5. Factor I

159




4.6. Factor B

159




4.7. Disease penetrance

160




5. Complement and Age-Related Macular Degeneration

160




5.1. Age-related macular degeneration

160




5.2. Factor H

161




5.3. Factor B/C2

163




6. Immunopathogenesis of aHUS and AMD

163




6.1. Atypical HUS

163




6.2. Age-related macular degeneration

166




7. Treatment of aHUS and AMD

167




7.1. Treatment options for aHUS

167




7.2. Treatment options for AMD

168




8. Conclusions: Lessons and Implications

168




References

169
5. Fc-Receptors as Regulators of Immunity179




Falk Nimmerjahn and Jeffrey V. Ravetch





1. Introduction

180




2. The Family of Activating and Inhibitory FcRs

181




3. Activating and Inhibitory FcR Signaling Pathways

183




4. The Role of Activating and Inhibitory FcRs on Innate Immune Effector Cells

185




5. Modulation of Antibody Activity

188




6. Activating and Inhibitory FcR Expression on DCs

190




7. Fc&famma;RIIB as a Master Regulator of Humoral Tolerance and Plasma Cell Survival

192




8. Summary and Outlook

195




Acknowledgments

196




References

196
Index205
Content of Recent Volumes211
Frederick W. Alt is a Howard Hughes Medical Institute (HHMI) Investigator and Director of the Program in Cellular and Molecular Medicine (PCMM) at Boston Children's Hospital (BCH). He is the Charles A. Janeway Professor of Pediatrics and Professor of Genetics at Harvard Medical School. He works on elucidating mechanisms that generate antigen receptor diversity and, more generally, on mechanisms that generate and suppress genomic instability in mammalian cells, with a focus on the immune and nervous systems. Recently, his group has developed senstive genome-wide approaches to identify mechanisms of DNA breaks and rearrangements in normal and cancer cells. He has been elected to the U.S. National Academy of Sciences, the U.S. National Academy of Medicine, and the European Molecular Biology Organization. His awards include the Albert Szent-Gyorgyi Prize for Progress in Cancer Research, the Novartis Prize for Basic Immunology, the Lewis S. Rosensteil Prize for Distinugished work in Biomedical Sciences, the Paul Berg and Arthur Kornberg Lifetime Achievement Award in Biomedical Sciences, and the William Silan Lifetime Achievement Award in Mentoring from Harvard Medical School.