Neuroprotective potential beyond immunoregulation of helminth infection as a therapeutic target in multiple sclerosis
| Autor: | Hai-Feng Li, Mei-Zeng Zhang, Xueqiang Hu, Wei Qiu, Xueping Zheng, Hong-Liang Zhang |
|---|---|
| Rok vydání: | 2011 |
| Předmět: |
Multiple Sclerosis
Helminthiasis Neuroprotection Schistosoma japonicum Immune system Th2 Cells Antigen Immunity Nerve Growth Factor medicine Animals Humans Nerve Growth Factors Autoimmune disease biology Multiple sclerosis Experimental autoimmune encephalomyelitis Models Immunological General Medicine Helminth Proteins medicine.disease biology.organism_classification Neuroprotective Agents nervous system Gene Expression Regulation Antigens Helminth Immunology Schistosoma mansoni |
| Zdroj: | Medical hypotheses. 78(1) |
| ISSN: | 1532-2777 |
| Popis: | Multiple sclerosis (MS) is a common disabling autoimmune disease in young adults which does not have an effective treatment. The prevalence of immune-mediated diseases is higher in developed countries with hygienic environments, suggesting that helminthic infection may protect from autoimmune diseases. Previously, we reported that soluble egg antigens (SEA) from Schistosoma japonicum suppressed experimental autoimmune encephalomyelitis (EAE), an animal model of MS, through up-regulating T helper-2 (Th2) immune responses in both the peripheral and central target organs. Neurotrophins (NTs) are not exclusive to the nervous system. While immune cells, especially Th2 cells, can produce and secrete a variety of NTs resulting in neuroprotective immunity. NTs can also modulate immune responses by augmenting Th2 responses and downregulating Th1 responses. Interestingly, nerve growth factor (NGF) has been found in liver granulomas of Schistosoma mansoni -infected mice. Moreover, in the central nervous system of chronic schistosomiasis, NGF is increased. A hypothesis is hereby proposed – SEA derived from S. japonicum bears neuroprotective properties beyond its immunomodulatory effects. SEA can induce the expression of NTs, which in turn augment Th2 immune responses induced by SEA; whereby a positive regulatory circuit between Th2 responses and NTs comes into being. |
| Databáze: | OpenAIRE |
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