PPARγ, a lipid-activated transcription factor as a regulator of dendritic cell function

Istvan Szatmari, Eva Rajnavolgyi, Laszlo Nagy

Research output: Chapter in Book/Report/Conference proceedingConference contribution

Abstract

In recent years it became apparent that PPARγ, besides being a key component of adipose tissue development and a target of insulin-sensitizing drugs, also has a role in immune cell differentiation and function. This receptor has been identified by us and others as a conductor of lipid handling in macrophages, and has roles also in inflammation control. Here we review recent advances on the role of this nuclear receptor in another key cell type of myeloid origin, dendritic cells (DCs). DCs are professional antigen-presenting cells having essential roles in antigen-uptake processing and presentation and in initiation of various forms of immune responses. It appears that PPARγ is expressed and is active in myeloid DCs and likely to be a regulator of DC function by altering antigen uptake, maturation, activation, migration, cytokine production, and lipid antigen presentation. Thus PPARγ is at the crossroads of lipid metabolism and innate immune response, and by studying its functions one has a unique opportunity to discern how these two seemingly distant fields (lipid metabolism and immune response) are interrelated. It is also possible that this receptor is a relevant target for pharmacological intervention in immune diseases such as chronic inflammation and autoimmune conditions.

Original languageEnglish (US)
Title of host publicationNeuroendocrine and Immune Crosstalk
PublisherBlackwell Publishing Inc.
Pages207-218
Number of pages12
ISBN (Print)1573316237, 9781573316231
DOIs
StatePublished - Jan 1 2006
Externally publishedYes

Publication series

NameAnnals of the New York Academy of Sciences
Volume1088
ISSN (Print)0077-8923
ISSN (Electronic)1749-6632

Fingerprint

Peroxisome Proliferator-Activated Receptors
Dendritic Cells
Antigen Presentation
Transcription Factors
Lipids
Myeloid Cells
Lipid Metabolism
Antigens
Inflammation
Macrophages
Immune System Diseases
Antigen-Presenting Cells
Cytoplasmic and Nuclear Receptors
Innate Immunity
Adipose Tissue
Cell Differentiation
Chemical activation
Pharmacology
Insulin
Tissue

Keywords

  • CD1
  • Dendritic cells
  • Innate immune response
  • Lipid metabolism
  • Nuclear hormone receptors
  • PPARγ
  • Transcription

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

Cite this

Szatmari, I., Rajnavolgyi, E., & Nagy, L. (2006). PPARγ, a lipid-activated transcription factor as a regulator of dendritic cell function. In Neuroendocrine and Immune Crosstalk (pp. 207-218). (Annals of the New York Academy of Sciences; Vol. 1088). Blackwell Publishing Inc.. https://doi.org/10.1196/annals.1366.013

PPARγ, a lipid-activated transcription factor as a regulator of dendritic cell function. / Szatmari, Istvan; Rajnavolgyi, Eva; Nagy, Laszlo.

Neuroendocrine and Immune Crosstalk. Blackwell Publishing Inc., 2006. p. 207-218 (Annals of the New York Academy of Sciences; Vol. 1088).

Research output: Chapter in Book/Report/Conference proceedingConference contribution

Szatmari, I, Rajnavolgyi, E & Nagy, L 2006, PPARγ, a lipid-activated transcription factor as a regulator of dendritic cell function. in Neuroendocrine and Immune Crosstalk. Annals of the New York Academy of Sciences, vol. 1088, Blackwell Publishing Inc., pp. 207-218. https://doi.org/10.1196/annals.1366.013
Szatmari I, Rajnavolgyi E, Nagy L. PPARγ, a lipid-activated transcription factor as a regulator of dendritic cell function. In Neuroendocrine and Immune Crosstalk. Blackwell Publishing Inc. 2006. p. 207-218. (Annals of the New York Academy of Sciences). https://doi.org/10.1196/annals.1366.013
Szatmari, Istvan ; Rajnavolgyi, Eva ; Nagy, Laszlo. / PPARγ, a lipid-activated transcription factor as a regulator of dendritic cell function. Neuroendocrine and Immune Crosstalk. Blackwell Publishing Inc., 2006. pp. 207-218 (Annals of the New York Academy of Sciences).
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