Th17 and Th22 Cells May Contribute To the Pathogenesis of Guillain-Barré Syndrome

Th17 cells

A study by Shujuan Li and colleagues from the Jilin University, Changchun, China, suggests that Th17 and Th22 cells might be involved in the onset and development of Guillain-Barré Syndrome.

Guillain-Barré syndrome (GBS), described in 1916 by George Guillain, Jean-Alexandre Barré, and André Strohl, is an acute inflammatory immune-mediated polyradiculoneuropathy presenting typically with tingling, progressive weakness, and pain.

Guillain-Barré syndrome is often a post-infectious, immune-mediated nerve injury, believed to be associated with Campylobacter jejuni, cytomegalovirus, Epstein-Barr virus, influenza A, Mycoplasma pneumoniae, Haemophilus influenzae, hepatitis (A, B, and E), and more recently, Zika virus infections.

Systemically and locally released cytokines appear to contribute to the pathogenesis of GBS, including cytokines such as interleukin (IL)-17 and IL-22. T helper (Th)17 cells and the IL-23→IL-17 axis drive chronic inflammation in many autoimmune diseases.

The report by Li et al, published in the journal Mediators of Inflammation, indicates that in the early, acute phase of Guillain-Barré syndrome circulating Th17, Th22 cells and Th1 cells are increased along with the plasma levels of IL-17 and IL-22.

Of note, intravenous immunoglobulin therapy (IVIg) treatment was able to down-regulate these cells and their cytokines at the plateau phase of GBS, and to attenuate clinical signs of GBS.

Interestingly, recent research indicates that IVIg inhibits the differentiation and amplification of Th17 cells and down-regulates IL-17A, IL-17F and IL-21 production.

The Mediators of Inflammation study may also indicate that targeting Th17 and Th22 cells may have therapeutic potential in Guillain-Barré syndrome.

In fact, a more recent review published in Expert Opinion on Therapeutic Targets provides a more detailed discussion along these lines.

Source: Mediators Inflamm, 2014:740947. doi: 10.1155/2014/740947. Epub 2014 May 12.
Read More: Mediators of Inflammation

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