Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) in central nervous system inflammation |
| |
Authors: | Olaf Hoffmann Frauke Zipp Joerg R Weber |
| |
Institution: | 1. Department of Neurology, Charité—Universit?tsmedizin Berlin, Berlin, Germany 2. Cecilie Vogt Clinic for Neurology, Charité—Universit?tsmedizin Berlin, Berlin, Germany 3. Department of Cell Biology and Neurobiology, Charité—Universit?tsmedizin Berlin, Berlin, Germany
|
| |
Abstract: | In a wide variety of acute and chronic central nervous system (CNS) disorders, inflammatory processes contribute to the damage
of brain cells and progression of the disease. Along with other regulatory cytokines, tumour necrosis factor-related apoptosis-inducing
ligand (TRAIL) is involved in the pathology of multiple sclerosis (MS) and murine experimental autoimmune encephalomyelitis
(EAE), bacterial meningitis (BM), HIV encephalitis (HIVE), stroke and Alzheimer's disease (AD). In these conditions, TRAIL
is released within the brain mainly by activated microglia and leukocytes infiltrating from the blood stream. TRAIL promotes
apoptosis of parenchymal cells in MS/EAE, HIVE, AD and stroke through interaction with TRAIL death receptors expressed on
these cells. Frequently, cells in the diseased brain display increased susceptibility to apoptosis induction by TRAIL due
to upregulation of death receptors and downregulation of decoy receptors. On the other hand, TRAIL inhibits the proliferation
of encephalitogenic T cells in EAE, and it is involved in the clearance of infected brain macrophages in HIVE and of activated
neutrophils in BM by interaction with their death receptors. Especially in BM, the ability of TRAIL to limit an acute granulocyte-driven
inflammation carries significant neuroprotective potential. Given the diversity of beneficial and harmful effects in the immune
and nervous system, TRAIL is a double-edged sword in diseases involving CNS inflammation. |
| |
Keywords: | TRAIL Cytokines Multiple sclerosis Meningitis Encephalitis Alzheimer's disease |
本文献已被 SpringerLink 等数据库收录! |
|