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Case Reports in Immunology
Volume 2014, Article ID 804761, 8 pages
Case Report

Increased IL-17, a Pathogenic Link between Hepatosplenic Schistosomiasis and Amyotrophic Lateral Sclerosis: A Hypothesis

1Division of Infectious Diseases, Ospedale Generale, 39100 Bolzano, Italy
2Division of Neurology, Ospedale Generale, 39100 Bolzano, Italy
3Radiology, Ospedale Generale, 39100 Bolzano, Italy
4Division of Hematology, Ospedale Generale, 39100 Bolzano, Italy
5Department of Experimental Medicine, Sapienza University, 00161 Rome, Italy

Received 13 April 2014; Accepted 15 July 2014; Published 23 July 2014

Academic Editor: Takahisa Gono

Copyright © 2014 Oswald Moling et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The immune system protects the organism from foreign invaders and foreign substances and is involved in physiological functions that range from tissue repair to neurocognition. However, an excessive or dysregulated immune response can cause immunopathology and disease. A 39-year-old man was affected by severe hepatosplenic schistosomiasis mansoni and by amyotrophic lateral sclerosis. One question that arose was, whether there was a relation between the parasitic and the neurodegenerative disease. IL-17, a proinflammatory cytokine, is produced mainly by T helper-17 CD4 cells, a recently discovered new lineage of effector CD4 T cells. Experimental mouse models of schistosomiasis have shown that IL-17 is a key player in the immunopathology of schistosomiasis. There are also reports that suggest that IL-17 might have an important role in the pathogenesis of amyotrophic lateral sclerosis. It is hypothesized that the factors that might have led to increased IL-17 in the hepatosplenic schistosomiasis mansoni might also have contributed to the development of amyotrophic lateral sclerosis in the described patient. A multitude of environmental factors, including infections, xenobiotic substances, intestinal microbiota, and vitamin D deficiency, that are able to induce a proinflammatory immune response polarization, might favor the development of amyotrophic lateral sclerosis in predisposed individuals.