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Prostaglandin E 2 is a negative regulator on human plasmacytoid dendritic cells
Author(s) -
Son Yonsu,
Ito Tomoki,
Ozaki Yoshio,
Tanijiri Tsutomu,
Yokoi Takashi,
Nakamura Kengo,
Takebayashi Masashi,
Amakawa Ryuichi,
Fukuhara Shirou
Publication year - 2006
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2006.02402.x
Subject(s) - regulator , microbiology and biotechnology , prostaglandin , prostaglandin e , chemistry , biology , endocrinology , biochemistry , gene
Summary Prostaglandin E 2 (PGE 2 ), a major lipid derived from the metabolism of arachidonic acid, is an environmentally bioactive substance produced by inflammatory processes and acts as a cAMP up‐regulator that plays an important role in immune responses. It has been reported that PGE 2 has the ability to inhibit the production of interleukin‐12 by myeloid dendritic cells (MDCs) and macrophages, and then induce preferential T helper type 2 (Th2) cell responses. However, little is known of the function of PGE 2 for plasmacytoid dendritic cells (PDCs), which may contribute to the innate and adaptive immune response to viral infection, allergy and autoimmune diseases. In the present study, we compared the biological effect of PGE 2 on human PDCs and MDCs. PGE 2 caused the death of PDCs but MDCs survived. Furthermore, we found that, whereas PGE 2 inhibited interferon‐α production by PDCs in response to virus or cytosine–phosphate–guanosine, it inhibited interelukin‐12 production by MDCs in response to lipopolysaccharide (LPS) or poly(I:C). Although both virus‐stimulated PDCs and LPS‐stimulated MDCs preferentially induced the development of interferon‐γ‐producing Th1 cells, pretreatment with PGE 2 led both DC subsets to attenuate their Th1‐inducing capacity. These findings suggest that PGE 2 represents a negative regulator on not only MDCs but also PDCs.