Expression of IL-5 and IL-13 by Th2 cells in experimental autoimmune encephalomyelitis

Date
2011
Authors
Perumalla, Danu Sicora
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Abstract

Multiple Sclerosis is considered an autoimmune disease where CD4 + T cells play an important role in promoting pathology. It affects approximately 2.5 million people in the world with approximately 400,000 of them in the US. There is no cure for the disease but treatments are available to manage symptoms and to prevent the progression of the disease. Although the exact cause of MS is unknown, it is believed that an imbalance between Th1 and Th2 cytokines within the CNS may promote or induce the disease. CD4 + T cells have been classified into different lineages such as Th1, Th2 and Th17 cells. Activated Th1 and Th17 cells produce proinflammatory cytokines such as IFN-gamma and IL-17 and are thought to promote autoimmune disease pathology. In contrast, Th2 cells produce cytokines such as IL-4, IL-5, IL-10 and IL-13 that are thought to regulate pathogenic effecter Th1 and Th17 cells. It has been suggested that Th2 cells producing IL-5 and/or IL-4 cannot inhibit pathogenic T cells directly in the CNS but may act in the periphery. However, it has not been addressed whether Th2 cells produce immunoregulatory IL-13 in the CNS at the site of autoimmune inflammation. Importantly, it has remained unresolved when or even if IL-13 and IL-5 are co-expressed.

Our results show production of IL-5 by Th2 cells in the CNS during EAE, but not IL-13. In contrast, IL-5 and IL-13 are produced by Th2 cells in the spleen. Our results suggest that IL-13 and IL-5 are being co-produced by CD4+T cell populations. Interestingly, it seems that there were no populations only expressing IL-13, but there were IL-5 single staining cells. This might suggest that some cells produce both cytokines and some only produce IL-5, or that at some later point the IL-5 and IL-13 double producing cells may produce less IL-13.

Overall, our results suggest that Th2 cells do not produce IL-13 in the CNS, which could explain why Th2 cells fail to inhibit autoimmune inflammation during EAE.

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Integrative Biology