VOLUME 3 | SEPTEMBER 2003 | 733 | Rick M. Maizels* and Maria Yazdanbakhsh†
The article discusses the immune regulation mechanisms employed by helminth parasites to downregulate host immunity, allowing them to survive and thrive in the host. Helminths, complex eukaryotic organisms, can live for decades in the human body and cause significant morbidity and disability. Despite this, many infected individuals remain asymptomatic, acting as long-term reservoirs for transmission. The article highlights the marked immunomodulatory effects of helminths, including both antigen-specific and generalized immune suppression. These effects are observed in human studies and animal models, where helminth infections lead to diminished responsiveness to antigens and reduced inflammatory responses.
The article also explores the role of T helper 2 (TH2) cells in helminth infections, noting that TH2 cells are often induced by helminths, leading to the production of immunoglobulin E (IgE) and other TH2 cytokines. However, the balance between TH1 and TH2 responses is complex, and the presence of regulatory T (Treg) cells is crucial for maintaining a balanced immune response. The article discusses the mechanisms by which helminths modulate the immune system, including the production of cytokines such as interleukin-10 (IL-10) and transforming growth factor-β (TGF-β), which can dampen both TH1 and TH2 responses.
Additionally, the article examines the role of dendritic cells (DCs) and other accessory cells in the immune response to helminths. DCs can be influenced by helminth molecules to promote TH2 responses and induce regulatory T cells. The article also reviews the immune modulators secreted by helminths, such as cystatins, prostaglandins, and glycans, which can interfere with antigen processing, modulate antigen-presenting cells, and block effector mechanisms.
Finally, the article discusses the potential for helminths to have evolved to stimulate TH2 cells for their own advantage, and the search for specific molecular patterns that mark helminths as pathogens. The article concludes by highlighting the ongoing research into the molecular mechanisms by which helminths modulate the host immune system and the potential implications for therapeutic interventions.The article discusses the immune regulation mechanisms employed by helminth parasites to downregulate host immunity, allowing them to survive and thrive in the host. Helminths, complex eukaryotic organisms, can live for decades in the human body and cause significant morbidity and disability. Despite this, many infected individuals remain asymptomatic, acting as long-term reservoirs for transmission. The article highlights the marked immunomodulatory effects of helminths, including both antigen-specific and generalized immune suppression. These effects are observed in human studies and animal models, where helminth infections lead to diminished responsiveness to antigens and reduced inflammatory responses.
The article also explores the role of T helper 2 (TH2) cells in helminth infections, noting that TH2 cells are often induced by helminths, leading to the production of immunoglobulin E (IgE) and other TH2 cytokines. However, the balance between TH1 and TH2 responses is complex, and the presence of regulatory T (Treg) cells is crucial for maintaining a balanced immune response. The article discusses the mechanisms by which helminths modulate the immune system, including the production of cytokines such as interleukin-10 (IL-10) and transforming growth factor-β (TGF-β), which can dampen both TH1 and TH2 responses.
Additionally, the article examines the role of dendritic cells (DCs) and other accessory cells in the immune response to helminths. DCs can be influenced by helminth molecules to promote TH2 responses and induce regulatory T cells. The article also reviews the immune modulators secreted by helminths, such as cystatins, prostaglandins, and glycans, which can interfere with antigen processing, modulate antigen-presenting cells, and block effector mechanisms.
Finally, the article discusses the potential for helminths to have evolved to stimulate TH2 cells for their own advantage, and the search for specific molecular patterns that mark helminths as pathogens. The article concludes by highlighting the ongoing research into the molecular mechanisms by which helminths modulate the host immune system and the potential implications for therapeutic interventions.