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Regulation of microglial activation by TGF‐β, IL‐10, and CSF‐1
Author(s) -
Lodge Patricia A.,
Sriram Subramaniam
Publication year - 1996
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.60.4.502
Subject(s) - microglia , biology , lipopolysaccharide , tumor necrosis factor alpha , immune system , secretion , proinflammatory cytokine , immunology , interleukin 10 , interleukin , endocrinology , inflammation , cytokine
Microglia are the resident macrophages of the brain and as such are active participants in immune responses in the central nervous system. Normal resting microglia express low levels of MHC class I and class II antigens and do not produce proinflammatory cytokines. However, microglial immune functions are induced in areas of infection or injury. To understand regulation of cytokines that are secreted by and act upon microglia, we examined production of interleukin (IL) ‐12, tumor necrosis factor‐α (TNF‐α), and nitric oxide (NO) by lipopolysaccharide (LPS)‐stimulated microglia. We observed secretion of IL‐12, TNF‐α, and NO following stimulation of microglia with LPS. Addition of IL‐10 suppressed TNF‐α, IL‐12, and NO production. Transforming growth factor‐β (TGF‐β) also inhibited TNF‐α and NO but did not affect IL‐12 secretion. IL‐12 secretion became sensitive to TGF‐β inhibition when microglia were cultured in the absence of CSF‐1. In addition to its effect on the response to TGF‐β, CSF‐1 suppressed the response of microglia to LPS. These data suggest that CSF‐1 may contribute to the immunologic ally privileged status of the central nervous system. J. Leukoc. Biol . 60: 502–508; 1996.