Ycoprotein that is predominantly expressed by activated T cells, B cells, myeloid cells, and platelets. It has been well established that CD40L upregulates the immune response by leading to increased CD4+ T cell activation; an effect which promotes the replication of HIV in infected lymphocytes and immune cells [104] and also that robust CD40 ligation promotes an inflammatory and neurotoxic enviro
S, a link between CD40 and microglia has been established. Upregulation of CD40 expression has been detected on microglia of HIV-1-infected brain tissues [28]. CD40L was also shown to potentiate the ability of HIV-1 Tat to activate monocytes and microglia leading to the overproduction of inflammatory proteins such as cytokines and chemokines [122]. Furthermore HAART is unable to modulate blood bra
S, a link between CD40 and microglia has been established. Upregulation of CD40 expression has been detected on microglia of HIV-1-infected brain tissues [28]. CD40L was also shown to potentiate the ability of HIV-1 Tat to activate monocytes and microglia leading to the overproduction of inflammatory proteins such as cytokines and chemokines [122]. Furthermore HAART is unable to modulate blood bra
The microglia signal transduction pathways mediating the neurotoxic response of Ab demonstrated that mitogen-activated protein-kinase (MAPK) superfamily members ERK1/2 and p38 MAPK act as mediators [95-97]. Furthermore, several lines of evidence indicate the NF-B in microglia is stimulated by b-amyloid [98,99]. Activation of NF-B can stimulate transcription of genes expressing TNF-a, IL-1, IL-6, m
Xins in both forms of dementia include TNF-a, arachidonic acid, platelet activating factors (PAF), nitric oxide (NO), and quinolinic acid (QUIN) [17,53-59]. Nitric oxide is synthesized by endothelial cells, neurons, and macrophages and is thought to be associated with NMDA-type glutamate-initiated neurotoxicity [54]. TNF-a is released by HIV-1-infected microglia, and oligodendrocytes are particula
Xins in both forms of dementia include TNF-a, arachidonic acid, platelet activating factors (PAF), nitric oxide (NO), and quinolinic acid (QUIN) [17,53-59]. Nitric oxide is synthesized by endothelial cells, neurons, and macrophages and is thought to be associated with NMDA-type glutamate-initiated neurotoxicity [54]. TNF-a is released by HIV-1-infected microglia, and oligodendrocytes are particula