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Gadd45 Stress Sensor Genes pp 51–68Cite as

Gadd45 Proteins in Immunity

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Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 793))

Abstract

The vertebrate immune system protects the host against invading pathogens such as viruses, bacteria and parasites. It consists of an innate branch and an adaptive branch that provide immediate and long-lasting protection, respectively. As the immune system is composed of different cell types and distributed throughout the whole body, immune cells need to communicate with each other. Intercellular communication in the immune system is mediated by cytokines, which bind to specific receptors on the cell surface and activate intracellular signalling networks. Growth arrest and DNA damage-inducible 45 (Gadd45) proteins are important components of these intracellular signalling networks. They are induced by a number of cytokines and by bacterial lipopolysaccharide. Within the innate immune system, Gadd45 proteins are crucial for the differentiation of myeloid cells as well as for the function of granulocytes and macrophages. Moreover, Gadd45β regulates autophagy, a catabolic pathway that also degrades intracellular pathogens. Regarding adaptive immunity, Gadd45 proteins are especially well characterized in T cells. For instance, Gadd45β and Gadd45γ regulate cytokine expression and Th1 differentiation, while Gadd45α inhibits p38 kinase activation downstream of the T cell receptor. Due to their many functions in the immune system, deficiency in Gadd45 proteins causes autoimmune diseases and less efficient tumour immunosurveillance.

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Abbreviations

ATG:

Autophagy-related

Bcl-xL :

B cell lymphoma x large

c-FLIP:

Cellular FLICE inhibitory protein

Cbl-b:

Casitas B-lineage lymphoma proto-oncogene b

CD:

Cluster of differentiation

CD4+ :

Cluster of differentiation 4-positive

CD8+ :

Cluster of differentiation 8-positive

CLR:

C-type lectin receptor

CR6:

Cytokine response gene 6

DISC:

Death-inducing signalling complex

EAE:

Experimental autoimmune encephalomyelitis

Egr:

Early growth response

G-CSF:

Granulocyte colony-stimulating factor

Gadd45:

Growth arrest and DNA damage 45

GM-CSF:

Granulocyte–macrophage colony-stimulating factor

GRAIL:

Gene related to anergy in lymphocytes protein

IFN:

Interferon

IL:

Interleukin

JNK:

c-Jun N-terminal kinase

LPS:

Lipopolysaccharide

M-CSF:

Macrophage colony-stimulating factor

MAPK:

Mitogen-activated protein kinase

MEKK4:

MAPK/ERK kinase kinase 4

MHC:

Major histocompatibility complex

MKK:

Mitogen-activated protein kinase kinase

MOG:

Myelin oligodendrocyte glycoprotein

Myd118:

Myeloid differentiation primary response protein 118

NFAT:

Nuclear factor of activated T cells

NF-κB:

Nuclear factor κB

NKT:

Natural killer T cell

NLR:

Nod-like receptor

PAMP:

Pathogen-associated molecular pattern

PRR:

Pattern recognition receptor

RLR:

Retinoic acid-inducible gene (RIG)-I-like receptor

ROS:

Reactive oxygen species

STAT:

Signal transducer and activator of transcription

TCR:

T cell receptor

TGF-β:

Transforming growth factor beta

Th:

T helper

TLR:

Toll-like receptor

TNFα:

Tumour necrosis factor alpha

TNFR1:

Tumour necrosis factor receptor 1

vMIA:

Viral mitochondrial-localized inhibitor of apoptosis

ZAP-70:

Zeta-chain associated protein of 70 kDa

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Acknowledgements

I am grateful to Dr. Yvonne Rauter and Alisha Walker for critically reading the manuscript and for helping with the figures. This work was supported by grants of the Deutsche Forschungsgemeinschaft (SCHM1586/3-1) and the Helmholtz Association cross-programme activity “Metabolic Dysfunction and Human Disease”.

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  1. Systems-Oriented Immunology and Inflammation Research, Helmholtz Center for Infection Research, Inhoffenstrasse 7, 38124, Braunschweig, Germany

    Ingo Schmitz

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Correspondence to Ingo Schmitz .

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Editors and Affiliations

  1. Professor of Biochemistry, Temple University School of Medicine, Philadelphia, Pennsylvania, USA

    Dan A. Liebermann

  2. Professor of Biochemistry, Temple University School of Medicine, Philadelphia, Pennsylvania, USA

    Barbara Hoffman

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Schmitz, I. (2013). Gadd45 Proteins in Immunity. In: Liebermann, D., Hoffman, B. (eds) Gadd45 Stress Sensor Genes. Advances in Experimental Medicine and Biology, vol 793. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-8289-5_4

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