Helminth protection against type-1 diabetes: an insight into immunomodulatory effect of helminth-induced infection.
Muhammad Adnan Sabir MughalMuhammad Kasib KhanZaheer AbbasRao Zahid AbbasHammad Ur Rehman BajwaAbdullah Khalid ChathaMuhammad ImranZia Ud Din SindhuAsghar AbbasArsalan ZafarMuhammad NadeemPublished in: Molecular biology reports (2021)
Helminths are the old dirty friends of humans from decades and may live undetected by the immune system for years in the tissues. They have evolved as good experts at subverting the immune system. Despite of their pathogenicity, they provide protection to their host against certain inflammatory diseases such as diabetes by modulating the immune mechanisms. These parasites are extra-cellular and induce Th2 response which triggers the adaptive immune cells as well as innate immune cells to work synergistically allowing Tregs to work in a toll-like receptor-dependent manure. T-helper cells type-2 also secrete certain anti-inflammatory cytokines including IL-4, IL-10, IL-13 and TGF-β which also provide protection against type-1 diabetes. Several helminths such as T. crassiceps, S. venezuelensis, filarial worms, Schistosoma spp. and T. spiralis have been reported to prevent diabetes in mouse models as well as in some clinical trials. Immunomodulatory talent of helminths is receiving greater attention to prevent diabetes. Herein, an attempt has been made to review and highlight the possible immuno-modulatory mechanisms by which helminths provide protection against diabetes. Moreover, this review also emphasizes on the use of helminth-derived molecules or synthetic derivatives of helminth-antigens in clinical trials to overcome rapidly growing autoimmune disorders including diabetes.
Keyphrases
- type diabetes
- glycemic control
- cardiovascular disease
- toll like receptor
- clinical trial
- immune response
- insulin resistance
- mouse model
- dendritic cells
- signaling pathway
- induced apoptosis
- multiple sclerosis
- escherichia coli
- regulatory t cells
- skeletal muscle
- cell death
- randomized controlled trial
- metabolic syndrome
- study protocol
- cell cycle arrest
- plasmodium falciparum
- open label
- phase iii
- endoplasmic reticulum stress
- pi k akt