Abstract:
:Considerable efforts have been invested to understand the mechanisms by which pro-inflammatory cytokines mediate the demise of β-cells in type 1 diabetes but much less attention has been paid to the role of anti-inflammatory cytokines as potential cytoprotective agents in these cells. Despite this, there is increasing evidence that anti-inflammatory molecules such as interleukin (IL)-4, IL-10 and IL-13 can exert a direct influence of β-cell function and viability and that the circulating levels of these cytokines may be reduced in type 1 diabetes. Thus, it seems possible that targeting of anti-inflammatory pathways might offer therapeutic potential in this disease. In the present review, we consider the evidence implicating IL-4, IL-10 and IL-13 as cytoprotective agents in the β-cell and discuss the receptor components and downstream signaling pathways that mediate these effects.
journal_name
Isletsjournal_title
Isletsauthors
Russell MA,Morgan NGdoi
10.4161/19382014.2014.950547subject
Has Abstractpub_date
2014-01-01 00:00:00pages
e950547issue
3eissn
1938-2014issn
1938-2022pii
950547journal_volume
6pub_type
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