Modulation of MHC Antigen Expression and Disease

Author: G. Eric Blair; Craig R. Pringle; D. John Maudsley  

Publisher: Cambridge University Press‎

Publication year: 2005

E-ISBN: 9780511888045

P-ISBN(Paperback): 9780521499217

Subject: R392.11 immune biology (the immunochemical fecal occult blood test)

Keyword: 医学免疫学

Language: ENG

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Modulation of MHC Antigen Expression and Disease

Description

The major histocompatibility complex (MHC) genes are involved in the immune system's response to tumour and infected cells and in generating an immune response. This book brings together basic aspects of the regulation of MHC antigens with important clinical applications (in viral infection, viral oncology, cancer biology and autoimmunity). There is a strong emphasis on situations where MHC expression is modulated (either stimulated or repressed). The book's major themes are: the mechanisms of MHC expression explored at several levels including the transcription and translation of MHC genes and the insertion of MHC protein molecules into plasma membranes; the effect of cytokines on MHC expression both in the aetiology of certain diseases and in possible immunotherapeutic approaches to disease; and the use of gene therapy to modify MHC expression in cancer cells, and thereby cause tumour rejection.

Chapter

2 Organization of the MHC

2.1 Introduction

2.2 The class I region

2.2.1 The human class I region

2.2.2 The mouse class I region

2.3 The class II region

2.3.1 The human class II region

2.3.2 The mouse class II region

2.4 The class III region

2.4.1 The human class III region

2.4.2 Comparison of the human and mouse class III regions

2.5 Conclusions

References

3 Interactions of cytokines in the regulation of MHC class I and class II antigen expression

3.1 Introduction

3.2 Tissue distribution of MHC antigens

3.3 General considerations in cytokine regulation of MHC expression

3.3.1 Interferon-γ

33.2 Alpha and beta interferons

3.3.3 Tumour necrosis factors

3.3.4 Interleukin-3

3.3.5 Interleukin-4

3.3.6 Interleukin-10

3.3.7 Colony-stimulating factors

3.3.9 Epidermal growth factor

3.3.10 Hormones and other factors

3.4 Effects of cytokines on MHC subregion expression

3.5 Evidence for cytokine modulation of MHC expression in vivo

3.6 Interactions of mediators in determining MHC expression

3.7 Conclusions: functional consequences of MHC class II modulation

Acknowledgement

References

4 Control of MHC class I gene expression

4.1 Introduction

4.2 The regulatory elements of MHC class I genes

4.3 Co-ordinated regulation of the MHC class I and the β-m genes

4.4 Trans-acting factors that bind to the cis elements in vitro

4.5 Factor binding to the MHC class I regulatory elements in vivo

4.6 Cloning of transcription factors that regulate MHC class I gene transcription

4.6.1 IFN regulatory factor (IRF)

4.6.2 NF-KB

4.6.4 RA induction of MHC class I transcription in N-Tera2 EC cells involves heterodimers ofRXR/5-RARp and NF-KB p50-p65

4.7 Conclusions

References

5 Control of MHC class II gene expression

5.1 Introduction

5.2 Role of the MHC class II antigens in the immune response

5.3 Normal tissue-specific and inducible patterns of MHC class II expression

5.4 Aberrant MHC class II expression and disease correlation

5.5 Lack of expression of MHC class II antigens leads to disease

5.6 Transcriptional control of eukaryotic genes

5.7 Molecular regulation of the MHC class II genes: DNA elements and transcription factors

5.8 Conclusions

References

6 Modulation of MHC antigen expression by viruses

6.1 Introduction

6.2 Modulation by viruses of MHC antigen expression is widespread

6.3 Mechanisms involved in modulating MHC antigen expression

6.4 Pathogenicity

6.5 Significance of viral traits

6.6 Evidence of modulation of MHC antigens in infections caused by non-viral pathogens

6.7 Conclusions

References

Note added in proof

7 Modulation of MHC antigen expression by retroviruses

7.1 Introduction

7.2 Murine leukaemia viruses

7.2.1. Moloney murine leukaemia virus

7.2.2 Radiation leukaemia virus

7.2.3 AKR/Gross leukaemia virus

7.2.4 Defective endogenous leukaemia viral sequences

7.2.5 Role of leukaemia virus induction of MHC antigens in leukaemogenesis

7.3 Murine sarcoma viruses and viral oncogenes

7.3.1 MHC regulation by ras and mos oncogenes

7.3.2 MHC regulation by the src oncogene

7.3.3 MHC regulation by the abl oncogene

7.3.4 MHC regulation by the fos oncogene

7.4 Human leukaemia and immunodeficiency viruses

7.4.1 Human T cell leukaemia virus

7.4.2 Human immunodeficiency virus (HIV)

Acknowledgements

References

8 Modulation of MHC class I antigen expression in adenovirus infection and transformation

8.1 Introduction

8.2 Molecular pathology of adenoviruses

8.2.1 Adenoviruses and human disease

8.2.2 Structure and assembly of adenoviruses

8.2.3 Expression of the adenovirus genome

8.2.4 Adenovirus transformation and oncogenicity

8.3 MHC class I antigen expression in adenovirus-transformed cells

8.3.1 Which immune effector cell(s) are responsible for rejecting cells transformed by non-oncogenic adenoviruses?

8.3.2 What is the mechanism of down-regulation ofMHC class I expression mediated by Adl2 ElA ?

8.4 MHC class I antigen expression in adenovirus-infected cells

8.4.1 Transcriptional regulation of class I expression in infected cells

8.4.2 Post-translational regulation of class I expression in infected cells

8.5 The effects of cytokines on MHC class I expression and immunomodulation in adenovirus infection and transformation

8.6 Conclusions

Acknowledgements

References

9 MHC expression in HPV-associated cervical cancer

9.1 Introduction

9.2 HPV expression in keratinocytes

9.3 MHC antigen expression in HPV 16-transfected keratinocytes

9.3.1 MHC class I expression

9.3.2 MHC class II expression

9.3.3 Cell-mediated lysis

9.4 Conclusions

Acknowledgements

References

10 Inhibition of the cellular response to interferon by hepatitis B virus polymerase

10.1 Introduction

10.2 Viral clearance in acute HBV infection

10.3 Viral persistence in chronic HBV infection

10.4 Interferon treatment in chronic HBV infections

10.5 Non-response to interferon: viral inhibition of the cellular response to interferon

10.6 Conclusions

References

11 Cellular adhesion molecules and MHC antigens in cells infected with Epstein-Barr virus: implications for immune recognition

11.1 Introduction: the CTL response to Epstein-Barr virus

11.2 Alternative EBV - host cell interactions

11.3 Modulation of cellular phenotype by EBV

11.4 BL as a model of escape from EBV-specific immunosurveillance

11.5 HLA class I expression by BL tumour cells

11.6 Conclusions

References

12 Effect of human cytomegalovirus infection on the expression of MHC class I antigens and adhesion molecules: potential role in immune evasion and immunopathology

12.1 Introduction

12.2 Effect of CMV infection on the expression of HLA class I on the surface of the infected cell

12.3 Effect of CMV infection on the cell surface expression of HLA class I on bystander uninfected cells

12.4 Intracellular expression of HLA class I in CMV-infected cells

12.5 Synthesis of HLA class I antigens in CMV-infected cells

12.6 Role of the CMV HLA class I homologue in the down-regulation of cell surface class I following CMV infection

12.7 Effect of CMV infection on the cell surface expression of adhesion molecules

12.8 Effect of CMV infection on leukocyte adhesion

12.9 Recognition of CMV-infected cells by MHC-restricted cytotoxic cells

12.10 Recognition of CMV-infected cells by non-MHC restricted cytotoxic cells

12.11 Conclusions

Acknowledgements

References

13 Oncogenes and MHC class I expression

13.1 Introduction: immune recognition of tumour cells

13.2 Modulation of MHC class I expression

13.2.1 Regulation of MHC class I expression in adenovirus-transformed cells

13.2.2 Regulation of MHC class I expression in tumour cells

13.3 Regulation of MHC class I expression by myc

13.3.1 The myc oncogenes

13.3.2 MHC class I down-modulation by myc

13.3.3 Locus-specific down-modulation by c-myc

13.3.4 Mechanism of down-regulation by myc

13.4 Biological consequences of myc activation

13.5 Conclusions

References

14 Mechanisms of tumour cell killing and the role of MHC antigens in experimental model systems

14.1 Introduction

14.2 Mechanisms of tumour-cell killing

14.2.1 Natural killer cells

14.2.2 MHC restricted cytotoxicity

14.2.3 Other mechanisms of tumour cell killing

14.2.4 Summary

14.3 Tumour immunogenicity

14.4 Restoration of MHC expression and tumorigenicity

14.4.1 MHC class I restoration

14.4.2 Allogeneic MHC class I gene transfection

14.4.3 MHC class II gene transfection

4.5 Conclusions

References

15 Manipulation of MHC antigens by gene transfection and cytokine stimulation: a possible approach for pre-selection of suitable patients for cytokine therapy

15.1 Introduction

15.1.1 MHC antigens and the immune system

15.1.2 MHC class I antigens and tumours

15.1.3 MHC class II antigens and tumours

15.2 MHC antigen expression in tumours and infiltration of T cells into tumours

15.3 Cytolytic activity and phenotypic profile of TILs

15.4 Expression of MHC antigens in tumour cell lines

15.4.1 MHC class I antigens

15.4.2 MHC class II antigens

15.5 Non-MHC-restricted tumour cell killing

15.6 Conclusions

Acknowledgements

References

16 Overexpression of MHC proteins in pancreatic islets: a link between cytokines, viruses, the breach of tolerance and insulindependent diabetes mellitus?

16.1 Introduction

16.1.1 The aberrant class II expression hypothesis of endocrine autoimmunity

16.1.2 Islet cell MHC expression in IDDM

16.2 Pathology of the islets in IDDM

16.2.1 HLA expression in the diabetic pancreas

16.2.2 Expression of adhesion molecules in the islets

16.2.3 Second signals

16.2.4 Cytokines

16.3 Induction of MHC expression in pancreatic islets cultured in vitro

16.3.1 Are there tissue-specific, strain-dependent differences in class II inducibility?

16.3.2 Is there defective class I expression in diabetes?

16.4 Viruses in human type 1 diabetes

16.4.1 Epidemiological and serological evidence

16.4.2 Difficulties in detecting viruses in the human islets

16.5 The NOD mouse

16.6 The BB rat

16.7 Virus-induced diabetes in rodents

16.8 Mice expressing transgenes in p cells

16.8.1 Expression ofisogeneic or allogeneic MHC products

16.8.2 Expression of cytokines

16.8.3 Mice expressing viral transgene products in the islets

16.8.4 Double and treble pins transgenic mice incorporating second signals

16.9 Conclusions

Acknowledgements

References

17 The role of cytokines in contributing to MHC antigen expression in rheumatoid arthritis

17.1 Introduction

17.2 HLA class II expression in RA synovium

17.3 Cytokine regulation of HLA class II expression

17.3.1 IFN-Y

17.3.2 GM-CSF

173.4 TNF-α

17.3.5 IL-4

17.3.6 IL-13

17.3.7 IL-10

17.3.8 TGF-β

11A Conclusions

References

18 Expression of an MHC antigen in the central nervous system: an animal model for demyelinating diseases

18.1 Introduction

18.2 Genetic susceptibility to MS

18.3 Viral involvement in MS

18.4 Autoimmune aspects of MS

18.5 An animal model for MS

References

Index

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