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Analysis of Human Natural Killer Cell Metabolism
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Natural killer T cells and ulcerative colitis.

Li Jie Lai1, Jun Shen1, Zhi Hua Ran1

  • 1State Key Laboratory for Oncogenes and Related Genes, Key Laboratory of Gastroenterology & Hepatology, Ministry of Health, Division of Gastroenterology and Hepatology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai Cancer Institute, Shanghai Institute of Digestive Disease, 160# Pu Jian Ave, Shanghai 200127, China.

Cellular Immunology
|January 15, 2019
PubMed
Summary

Natural killer T (NKT) cells and cytokines like IL-13, IL-5, and IL-4 play key roles in ulcerative colitis (UC) pathogenesis. Targeting these elements offers potential new therapies for this inflammatory bowel disease (IBD).

Keywords:
CytokinesNatural killer T cellsPathogenesisTherapeuticsUlcerative colitis

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Area of Science:

  • Immunology
  • Gastroenterology
  • Inflammatory Bowel Disease Research

Background:

  • Ulcerative colitis (UC), a major form of inflammatory bowel disease (IBD), involves aberrant innate and adaptive immunity.
  • The digestive tract's abnormal inflammation and immune responses are central to UC pathogenesis.
  • Natural killer T (NKT) cells are implicated in both innate and adaptive immunity, interacting with various cytokines.

Purpose of the Study:

  • To review the roles of NKT cells and associated cytokines in the development of UC.
  • To explore the potential of manipulating NKT cells for immune response reconstruction in UC.
  • To discuss novel therapeutic strategies targeting NKT cells and their cytokines for UC treatment.

Main Methods:

  • Literature review focusing on NKT cells and cytokine involvement in UC.
  • Analysis of recent studies on the roles of IL-13, IL-5, and IL-4 in UC.
  • Examination of therapeutic approaches including neutralizing antibodies and cytokine inhibitors.

Main Results:

  • NKT cells and specific cytokines (IL-13, IL-5, IL-4) are significantly involved in UC occurrence and progression.
  • Aberrant immune responses in UC are linked to the dysregulation of NKT cells and cytokine signaling.
  • Targeting NKT cells and their cytokine products presents promising therapeutic avenues for UC.

Conclusions:

  • NKT cells and cytokines are critical players in the immunopathogenesis of ulcerative colitis.
  • Modulating NKT cell activity and cytokine pathways offers potential for novel UC therapies.
  • Neutralizing antibodies and inhibitors targeting NKT cell-derived cytokines represent emerging treatment options for UC.