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The Role of IL-10 in Regulating Immunity to Persistent Viral Infections

Chapter
Part of the Current Topics in Microbiology and Immunology book series (CT MICROBIOLOGY, volume 350)

Abstract

The immune system has evolved multipronged responses that are critical to effectively defend the body from invading pathogens and to clear infection. However, the same weapons employed to eradicate infection can have caustic effects on normal bystander cells. Therefore, tight regulation is vital and the host must balance engendering correct and sufficient immune responses to pathogens while limiting errant and excessive immunopathology. To accomplish this task, a complex network of positive and negative immune signals are delivered, which in most instances successfully eliminate the pathogen. However, in response to some viral infections, immune function is rapidly suppressed leading to viral persistence. Immune suppression is a critical obstacle to the control of many persistent viral infections such as HIV, hepatitis C, and hepatitis B virus, which together affect more than 500 million individuals worldwide. Thus, the ability to therapeutically enhance immunity is a potentially powerful approach to resolve persistent infections. The host-derived cytokine IL-10 is a key player in the establishment and perpetuation of viral persistence. This chapter discusses the role of IL-10 in viral persistence and explores the exciting prospect of therapeutically blocking IL-10 to increase antiviral immunity and vaccine efficacy.

Keywords

Human Immunodeficiency Virus Human Immunodeficiency Virus Infection Persistent Infection Viral Persistence Human Immunodeficiency Virus Replication 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Notes

Acknowledgments

Our work was supported by the UCLA Center for AIDS Research, the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA, the Johanna and Joseph Shaper Family Chair, and grants from the National Institutes of Health (AI082975, AI085043 to D.G.B.).

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© Springer-Verlag Berlin Heidelberg 2010

Authors and Affiliations

  1. 1.Department of Microbiology, Immunology and Molecular Genetics and the UCLA AIDS Institute, David Geffen School of MedicineUniversity of CaliforniaLos AngelesUSA

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