Communication is key: Innate immune cells regulate host protection to helminths

Abstract

Parasitic helminth infections remain a significant global health issue and are responsible for devastating morbidity and economic hardships. During infection, helminths migrate through different host organs, which results in substantial tissue damage and the release of diverse effector molecules by both hematopoietic and non-hematopoietic cells. Thus, host protective responses to helminths must initiate mechanisms that help to promote worm clearance while simultaneously mitigating tissue injury. The specialized immunity that promotes these responses is termed type 2 inflammation and is initiated by the recruitment and activation of hematopoietic stem/progenitor cells, mast cells, basophils, eosinophils, dendritic cells, neutrophils, macrophages, myeloid-derived suppressor cells, and group 2 innate lymphoid cells. Recent work has also revealed the importance of neuron-derived signals in regulating type 2 inflammation and antihelminth immunity. These studies suggest that multiple body systems coordinate to promote optimal outcomes post-infection. In this review, we will describe the innate immune events that direct the scope and intensity of antihelminth immunity. Further, we will highlight the recent progress made in our understanding of the neuro-immune interactions that regulate these pathways and discuss the conceptual advances they promote.

A Myeloid-Specific Lack of IL-4Rα Prevents the Development of Alternatively Activated Macrophages and Enhances Immunity to Experimental Cysticercosis

“…The immune response against parasite helminths, where myeloid cells play essential roles in inducing protection in the host, has been described widely. Mast cells, basophils, dendritic cells, neutrophils, monocytes, and macrophages have prominent roles whereby IL-4/IL-13 polarizing cytokines participate in resolving the infection in favor of the host [ 20 ]. Basophils promote intestinal helminth clearance, inducing increased amounts of IL-4 and prostaglandins, favoring the antigen presentation to T-CD4 + cells, and promoting the development of M2 macrophages to repair the damaged tissues [ 20 , 21 ].…”

“…Mast cells, basophils, dendritic cells, neutrophils, monocytes, and macrophages have prominent roles whereby IL-4/IL-13 polarizing cytokines participate in resolving the infection in favor of the host [ 20 ]. Basophils promote intestinal helminth clearance, inducing increased amounts of IL-4 and prostaglandins, favoring the antigen presentation to T-CD4 + cells, and promoting the development of M2 macrophages to repair the damaged tissues [ 20 , 21 ]. Another source of IL-4, essential to generating M2 macrophages during helminth infections, is the T-CD4 + lymphocyte, where the synergy between T cells and group 2 innate lymphoid cells (ILC2) for IL-13 production has been described [ 22 ].…”

A mast cell-related prognostic model for non-small cell lung cancer

“…MCs are known for their biological role in allergic reactions but are also now known to be involved in many other important physiological and pathological processes ( 27 , 28 ). MC infiltration has also been found in some human and animal tumor models; however, its function in the tumor microenvironment remains controversial ( 26 , 29 ). Further studies of the role of MCs in NSCLC are warranted.…”

mmu-miR-374b-5p modulated inflammatory factors via downregulation of C/EBP β/NF-κB signaling in Kupffer cells during Echinococcus multilocularis infection

“…Subsequently, Th1-type immune response gradually changes to the Th2-type immune response, which is contributed to survive for the worms in host. And some researchers [32,33] found that in the early stage of worm infection, anti-in ammatory factors showed an upward trend. Our research results also support this statement.…”