In the central nervous system (CNS) microglia are crucial for the defense of the brain against invading microorganisms,
formation of tumors, and damage following trauma . However, uncontrolled activation of these cells may
have deleterious outcomes  through activation of Fcγ and the complement 3 receptors and the induction of an adaptive
immune reaction . Proteins contributing to this reaction are the intercellular adhesion molecule-1 (ICAM-1)  and
CD3 molecules, among others. Both can be expressed on the glia cells before cytokine release and may facilitate an autoimmune
inflammatory reaction in the brain. Round microglial cells among the pyramidal cells of the hippocampus with
increased expression of CD32+ (FcγIIa) and near the site of injection of aluminum were detected immunohistochemically
and indicate microglial activation at the site of aluminum injury. ICAM-1+ immunoreactivity significantly increased in the
hippocampus and in the choroids plexus, indicating increased inflammation in the brain as well as increased CD3ع+ expression
in the hippocampus and non-MHC-restricted T cytotoxicity after aluminum injection.
The pattern of expression of CD32+ (FcIIa receptor) near the site of aluminum injection indicates that microglia may play
a phagocytic role at the site of aluminum-induced excitotoxicity in the brain. Significant expression of ICAM-1+ and
CD3ع+ immunoreactive cells with the clusters of ICAM-1+ in the choroid plexus suggests a consequently neurotoxic autoimmune
reaction induced by microglial hyperactivation in the injured brain.
Keywords: Aluminum excitotoxicity, neuroautoimmunity, CD32, ICAM-1, CD3ع, Brain Aging, central nervous system, trauma, Fcγ, glia cells
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