Apoptosis: A target for potentiation of UV-induced IL-1Ra synthesis by IVIg

Craciun, Ligia; Digiambattista, M.; Laub, R; Goldman, Michel; Dupont, Étienne

doi:10.1016/j.imlet.2007.02.010

Cited by 6 publications

(5 citation statements)

References 42 publications

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“…Surprisingly, anti-inflammatory activity was associated only with sialylated Fab. IVIG may also reduce inflammation by inducing the release of interleukin-10 [ 104 ] and IL-1 receptor antagonist (IL-1ra) [ 105 ], both of which have anti-inflammatory actions [ 106 ].…”

Section: Reviewmentioning

confidence: 99%

Should development of Alzheimer’s disease-specific intravenous immunoglobulin be considered?

Loeffler

2014

J Neuroinflammation

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Recent phase II and III studies with intravenous immunoglobulin (IVIG) in patients with Alzheimer’s disease (AD) did not find evidence for the slowing of AD progression compared to placebo-treated patients, in contrast to encouraging results in pilot studies. An additional phase III trial is ongoing. If negative results are found, then further AD studies with IVIG are unlikely unless a manufacturer opts for a trial with high-dose IVIG, which would increase its anti-inflammatory effects but also the risk for adverse events. An alternative approach could be an AD-specific IVIG, supplementing IVIG with higher concentrations of selected antibodies purified from it or produced via recombinant polyclonal antibody technology. These antibodies could include those to amyloid-beta (Aβ, tau protein, inflammatory cytokines, complement activation proteins, and the receptor for advanced glycation end products. IgG fragment crystallizable (Fc) fragments containing terminal sialic acid could be added to increase anti-inflammatory effects. While this product might be more effective in slowing AD clinical progression than current IVIG, there are difficulties with this approach. Preclinical studies would be required to determine which of the antibodies of interest for supplementing current IVIG (for example, antibodies to phosphorylated or oligomeric tau) are actually present (and, therefore, available for purification) in IVIG, and the effects of the product in mouse models of AD. An Investigational New Drug application for an AD-specific IVIG would require United States Food and Drug Administration approval. If the drug would be found to benefit AD patients, meeting the increased demand for IVIG would be challenging.

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Section: Reviewmentioning

confidence: 99%

Should development of Alzheimer’s disease-specific intravenous immunoglobulin be considered?

Loeffler

2014

J Neuroinflammation

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“…To induce apoptosis, the cells in uncovered dishes were exposed to UVB radiation. The exposure time of 11 min and a distance of 4 cm from the source (20W/12 lamp emitting 2.1 W at 257 nm) produced the maximum percentage of apoptotic cells detected by microscope (17)(18).…”

Section: Apoptosis Detectionmentioning

confidence: 99%

Antioxidant micronutrients improve intrinsic and UV-induced apoptosis of human lymphocytes particularly in elderly people

Ge²,

Zhang

et al. 2011

The Journal of nutrition, health and aging

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“…Modulation of cytokines and cytokine antagonists by IVIG is another major mechanism by which immunoglobulin exerts its anti-inflammatory effects. IVIG was shown to selectively trigger the production of IL-1 receptor antagonist (IL-1ra), the natural antagonist of IL-1 (Craciun et al, 2007; Crow et al, 2007). There is also evidence to indicate that IVIG causes down-regulation of endothelial cell intercellular adhesion molecules ICAM-I, and lymphocyte function-associated antigen-1 (LFA-1) on activated T-cells (Rigal et al, 1994).…”

Section: Mechanisms Of Actions Of Intravenous Immunoglobulinmentioning

confidence: 99%

Neuroprotection in stroke by complement inhibition and immunoglobulin therapy

et al. 2009

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Activation of the complement system occurs in a variety of neuroinflammatory diseases and neurodegenerative processes of the CNS. Studies in the last decade have demonstrated that essentially all of the activation components and receptors of the complement system are produced by astrocytes, microglia, and neurons. There is also rapidly growing evidence to indicate an active role of the complement system in cerebral ischemic injury. In addition to direct cell damage, regional cerebral ischemia and reperfusion (I/R) induces an inflammatory response involving complement activation and generation of active fragments, such as C3a and C5a anaphylatoxins, C3b, C4b, and iC3b. The use of specific inhibitors to block complement activation or their mediators such as C5a, can reduce local tissue injury after I/R. Consistent with therapeutic approaches that have been successful in models of autoimmune disorders, many of the same complement inhibition strategies are proving effective in animal models of cerebral I/R injury. One new form of therapy, which is less specific in its targeting of complement than monodrug administration, is the use of immunoglobulins. Intravenous immunoglobulin (IVIG) has the potential to inhibit multiple components of inflammation, including complement fragments, pro-inflammatory cytokine production and leukocyte cell adhesion. Thus, IVIG may directly protect neurons, reduce activation of intrinsic inflammatory cells (microglia) and inhibit transendothelial infiltration of leukocytes into the brain parenchyma following an ischemic stroke. The striking neuroprotective actions of IVIG in animal models of ischemic stroke suggest a potential therapeutic potential that merits consideration for clinical trials in stroke patients.

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Apoptosis: A target for potentiation of UV-induced IL-1Ra synthesis by IVIg

Cited by 6 publications

References 42 publications

Should development of Alzheimer’s disease-specific intravenous immunoglobulin be considered?

Should development of Alzheimer’s disease-specific intravenous immunoglobulin be considered?

Antioxidant micronutrients improve intrinsic and UV-induced apoptosis of human lymphocytes particularly in elderly people

Neuroprotection in stroke by complement inhibition and immunoglobulin therapy

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