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Helicobacter pylori: Immune Responses and Gastric Autoimmunity

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The Microbiome in Rheumatic Diseases and Infection

Abstract

Helicobacter pylori infects almost half of the population worldwide. H. pylori induces the activation of a fascinating cytokine and chemokine network in the gastric mucosa. Chronic H. pylori infection represents a very interesting model of how a single bacterial infection might result in a variety of different clinical outcomes such as duodenal and gastric ulcers, gastric adenocarcinoma, autoimmune gastritis and B cell lymphoma of mucosa-associated lymphoid tissue. The type of host immune response against H. pylori, particularly the cytolytic effector functions of T cells, is crucial for the outcome of the infection. T cells are potentially able to kill a target via different mechanisms, such as perforins or Fas-Fas ligand interaction. In H. pylori-infected patients with gastric autoimmunity, cytolytic T cells that cross-recognize different epitopes of H. pylori proteins and H(+)K(+)-ATPase autoantigen infiltrate the gastric mucosa and lead to gastric atrophy via long-lasting activation of Fas ligand-mediated apoptosis and perforin-induced cytotoxicity. This chapter will focus on the innate immune responses and the role of H. pylori, T cells and cytokines in the onset of autoimmune gastritis.

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Abbreviations

AIG:

Autoimmune gastritis

AP:

Activating protein-1

ATPase:

Adenosine triphosphatase

CagA:

Cytotoxin-associated protein

cagPAI:

cag pathogenicity island

E. coli :

Escherichia coli

EAIG:

Experimental autoimmune gastritis

FasL:

Fas ligand

GlcNAc-MurNAc:

N-Acetyl glucosamine-N-acetyl muramic acid

H. pylori :

Helicobacter pylori

HBD:

Human beta-defensin

HLA:

Human leukocyte antigen

HP0175:

Secreted peptidyl prolyl cis, trans-isomerase of H. pylori

HP-NAP:

H. pylori neutrophil-activating protein

IFN:

Interferon

IL:

Interleukin

IRF:

IFN regulatory factor

IRFs:

Interferon regulatory factors

ISGs:

Interferon-stimulated genes

LPS:

Lipopolysaccharide

MALT:

Mucosal-associated lymphoid tissue

MAMP:

Microbe-associated molecular pattern

MAPK:

Mitogen-activated protein kinase

MCP:

Monocyte chemotactic protein

mDAP:

Meso-diaminopimelate

MMP:

Matrix metalloproteinase

NF-κB:

Nuclear factor transcription beta

NLR:

Nod-like receptor

NOD:

Nucleotide-binding oligomerization domain

OMVs:

Outer membrane vesicles

PA:

Pernicious anaemia

PgdA:

Peptidoglycan deacetylase

PRR:

Pathogen recognition receptor

RIG:

Retinoic acid-inducible gene

TCR:

T cell receptor

Th:

T helper

TILs:

Tumour-infiltrating lymphocytes

TLR:

Toll-like receptor

TNF:

Tumour necrosis factor

VacA:

Vacuolating cytotoxin A

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Correspondence to Mario M. D’Elios .

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Kaparakis-Liaskos, M., D’Elios, M.M. (2018). Helicobacter pylori: Immune Responses and Gastric Autoimmunity. In: Ragab, G., Atkinson, T., Stoll, M. (eds) The Microbiome in Rheumatic Diseases and Infection. Springer, Cham. https://doi.org/10.1007/978-3-319-79026-8_8

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