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IL-4 inhibits the expression of mouse formyl peptide receptor 2, a receptor for amyloid beta(1-42), in a TNF-alpha-Activated microglia

  1. Author:
    Iribarren, P.
    Chen, K. Q.
    Hu, J. Y.
    Zhang, X.
    Gong, W. H.
    Wang, J. M.

  2. Author Address

    NCI, Mol Immunoregulat Lab, Ctr Canc Res, Frederick, MD 21702 USA. NCI, Expt Immunol Lab, Ctr Canc Res, Frederick, MD 21702 USA. SAIC Frederick, Basic Res Program, Ft Detrick, MD 21702 USA Wang, JM, NCI, Mol Immunoregulat Lab, Ctr Canc Res, Bldg 560,Room 31-40, Frederick, MD 21702 USA
    1. Year: 2005
    2. Date: NOV 1
  2. Journal: Journal of Immunology
    1. 175
    2. 9
    3. Pages: 6100-6106
  4. Type of Article: Article
  1. Abstract:

    Microglia are phagocytic cells in the CNS and actively participate in proinflammatory responses in neurodegenerative diseases. We have previously shown that TNF-alpha up-regulated the expression of formyl peptide receptor 2 (mFPR2) in mouse microglial cells, resulting in increased chemotactic responses of such cells to mFPR2 agonists, including amyloid beta(1-42) (A beta(42)), a critical pathogenic agent in Alzheimer's disease. In the present study, we found that IL-4, a Th2-type cytokine, markedly inhibited TNF-alpha-induced expression of mFPR2 in microglial cells by attenuating activation of ERK and p38 MAPK as well as NF-kappa B. The effect of IL-4 was not dependent on Stat6 but rather required the protein phosphatase 2A (PP2A) as demonstrated by the capacity of PP2A small interfering RNA to reverse the effect of IL-4 in TNF-alpha-activated microglia. Since both IL-4 and TNF-alpha are produced in the CNS under pathophysiological conditions, our results suggest that IL-4 may play an important role in the maintenance of CNS homeostasis by limiting microglial activation by proinflammatory stimulants

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External Sources

  1. View record in Web of Science®
  2. WOS: 000232786300068

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