We know that the IFNβ is often used as an anti-inflammatory. Does IFNβ play a role in proinflammation? Especially in autoimmunity?
Neuromyelitis optica (NMO) is an antibody mediated disease that can present similarly to Multiple sclerosis. In some instances interferon B has been given to patients with NMO and a worsening of the symptoms has been noted in a couple of publications (Palace J, Leite MI, Nairne A, Vincent A. Arch Neurol. 2010 Aug;67(8):1016-7; Warabi Y, Matsumoto Y, Hayashi H.
J Neurol Sci. 2007 Jan 15;252(1):57-61.) Others suggest interferon B increases levels of BAFF which may provide an explanation for this worsening in an antibody mediated disease (Gandhi KS, McKay FC, Schibeci SD, Arthur JW, Heard RN, Stewart GJ, Booth DR.
J Interferon Cytokine Res. 2008 Sep;28(9):529-39.)
I think that the beneficial or harmful action of any cytokine is context-specific. Administration of soluble cytokines will not work as anticipated since they have short half lives in vivo and they can act on every cell type in the body unlike in vitro. There are numerous examples of contraindications of cytokines. IL-2 and GM-CSF are good examples. Perhaps localized delivery of cytokines proven to have specific effects in whole experimental animals and not in tissue culture may have the potential to provide benefits to humans.
Autoimmune diseases employ different mechanisms which are not fully understood. For instance, type 1 diabetes involves destruction of insulin-producing beta cells by still unknown mechanisms. In this instance, neutrophils are not involved. Macrophages, dendritic cells, B cells and T lymphocytes have been implicated. Among them, T-cells play a major role. So, IFN-beta may be beneficial in some but not in all cases. So, we have to address issues specifically.
It is interesting to learn that IFN-beta administration has worse outcome in NMO cases. This is similar to anti-TNF-alpha therapy not providing protection against MS in some patients. A recent paper has elegant explanation for this: Gregory et al. Nature. 2012; 488:508.
Certainly appears to in dermatomyositis. A recent study at http://ard.bmj.com/content/70/5/831.abstract in the EULAR journal shows strongly elevated IFN-beta in dermatomyositis patients
IFN-beta inducible proteins such as the p200-family proteins mediate both pro and anti-inflammatory activities. Further, the ratio between levels of certain p200-family proteins determines the outcome of the IFN response.
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