Helicobacter pylori neutrophil activating protein's potential as tool in therapeutic immune modulation

Victor Reyes, Ellen J. Beswick

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Helicobacter pylori is one of the most common human pathogens and is associated with chronic gastritis, peptic ulcers and gastric carcinoma. H. pylori establishes a persistent infection, suggesting that the host response is ineffective in clearing the infection. H. pylori employs multiple mechanisms to undermine host responses. For example, CD4+ T cells are recruited to the gastric mucosa of infected individuals, but these cells are predominantly T helper 1 (TH1) cells, which do not provide protection from the extracellular pathogen. H. pylori neutrophil-activating protein (HP-NAP) promotes the TH1 polarized response. HP-NAP induces macrophages and dendritic cells to produce IL-12 and IL-23, which could explain the effect on T cells. These properties of HP-NAP make it a potential immunotherapeutic tool to redirect harmful TH2 cell responses, as seen in atopic allergy, to TH1 cell responses and also in IL-12 induction in cancer therapy.

Original languageEnglish (US)
Pages (from-to)1315-1320
Number of pages6
JournalExpert Opinion on Therapeutic Patents
Volume17
Issue number10
DOIs
StatePublished - Oct 2007

Fingerprint

helper
Helicobacter pylori
Th1 Cells
Interleukin-12
Interleukin-23
T-Lymphocytes
allergy
Gastritis
Gastric Mucosa
Infection
Peptic Ulcer
induction
Dendritic Cells
Stomach
Hypersensitivity
cancer
Therapeutics
Macrophages
Carcinoma
Helicobacter pylori neutrophil-activating protein A

Keywords

  • Adjuvant
  • Atopy
  • Cytokines
  • Helicobacter pylori
  • Immune modulation
  • T cells

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Pharmacology
  • Law

Cite this

Helicobacter pylori neutrophil activating protein's potential as tool in therapeutic immune modulation. / Reyes, Victor; Beswick, Ellen J.

In: Expert Opinion on Therapeutic Patents, Vol. 17, No. 10, 10.2007, p. 1315-1320.

Research output: Contribution to journalArticle

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