Tissue-specific immunity in helminth infections

Abstract

A characteristic feature of host responses to helminth infections is the development of profound systemic and tissue-localised Type 2 immune responses that play critical roles in immunity, tissue repair and tolerance of the parasite at tissue sites. These same Type 2 responses are also seen in the tissue-associated immune-pathologies seen in asthma, atopic dermatitis and many forms of allergies. The recent identification of new subtypes of immune cells and cytokine pathways that influence both immune and non-immune cells and tissues creates the opportunity for reviewing helminth parasite–host responses in the context of tissue specific immunity. This review focuses on the new discoveries of the cells and cytokines involved in tissue specific immune responses to helminths and how these contribute to host immunity against helminth infection and allow the host to accommodate the presence of parasites when they cannot be eliminated.

Trickle infection with Heligmosomoides polygyrus results in decreased worm burdens but increased intestinal inflammation and scarring

“…Using our trickle model, C57Bl/6 mice had fewer worms than those infected with a single bolus infection. Resilience to a bolus H. polygyrus infection has been attributed to a strong Th2 response, requiring tuft cells activation, Th2 cytokine production (IL-4 and 13 in particular), the formation of granulomas, IgG1 production, and the activation of alternatively activated macrophages and mast cells ( 3 , 66 ). Other changes in intestinal physiology and immune markers have also been observed but not directly linked to resilience ( 3 , 66 ).…”

“…Resilience to a bolus H. polygyrus infection has been attributed to a strong Th2 response, requiring tuft cells activation, Th2 cytokine production (IL-4 and 13 in particular), the formation of granulomas, IgG1 production, and the activation of alternatively activated macrophages and mast cells ( 3 , 66 ). Other changes in intestinal physiology and immune markers have also been observed but not directly linked to resilience ( 3 , 66 ). In our model, despite the reduced parasite numbers in trickle-infected animals, we were surprised that many of the resilience-associated parameters were unchanged, especially since previous studies using H. polygyrus trickle infection models have linked resilience to increased Il4 expression levels in the MLN and increased serum IgG1 ( 41 , 67 ).…”

The Potential Role of Microorganisms on Enteric Nervous System Development and Disease

“…Helminth infection triggers type 2 immune responses by releasing interleukin (IL)-4, IL-5, and IL-13 from innate lymphoid cells type 2 (ILC2) to CD4 + T cells (Th2), which function to accelerate parasite expulsion via the ‘weep and sweep’ response. Thus, parasitic infestation could potentially also alter or modulate the ENS [ 125 , 126 ].…”

Functional Recognition Theory and Type 2 Immunity: Insights and Uncertainties

“…Type 2 immunity evolved, in part, to provide host protection against parasitic helminths, including either mediating parasite expulsion or tolerance to the helminth in peripheral tissues (23). For instance, in mice, Nippostrongylus brasiliensis primary expulsion and Heligmosomoides polygyrus secondary expulsion require CD4 1 Th2 cells (24).…”