How the Body Stops the Type 2 Immune Response and Onset of Allergic Disease

SUPPRESSION of group 2 innate lymphoid (IL2) cells following infection has been shown to prevent the innate immune response from continuing when it is no longer needed, according to research from the RIKEN Center for Integrative Medical Sciences (IMS) in Japan.

IL2 cells are long-lived, Type 2 cytokine-producing cells of the innate immune system that play important roles in fighting helminth infection and allergic inflammation. Helminths present a substantial challenge to human health and are a major cause of mortality in the developing world. The body’s primary defence against helminths, in addition to some fungal infections, is the Type 2 innate immune response.

Though it was previously believed that the response was mainly mounted by short-lived cells, it is now accepted that it actually involves the longer-lived IL2 cells; this leads to a cost to the response system, as persistence of the immune response may lead to allergic inflammatory responses, such as those in asthma. This association means that it is important to understand the mechanism by which IL2 cells are suppressed.

The study, which looked at lung inflammation induced by infection with Alternaria alternata, a known risk factor for asthma, found that IL2 cells are switched off by the cytokines interferon-beta, interferon-gamma, and interleukin-27, which ends the immune response. The researchers also demonstrated that IL2 cells permanently reside in body tissues and are activated when a threat is detected, as opposed to migrating to specific tissues when an immune response is required, showing that the response is mounted in a very locally specific way; this may be another way in which the body prevents the ongoing inflammation that can be associated with this response.

Team leader Dr Shigeo Koyasu, Group Director, Laboratory for Immune Cell Systems, IMS, Wako, Japan, summarised: “These findings are helpful in understanding how the Type 2 innate response changes to be both beneficial and harmful. Learning how these cells are activated and inactivated can give us clues for understanding and treating how the body reacts to such infections.”

He added: “We are beginning to gain insights into the innate immune response, which was previously thought to be simpler than our understanding today. I hope that our work will encourage researchers to look for similar regulatory mechanisms in Type 1 and Type 3 innate immune responses as well, as this will help us to gain a broader understanding of the complexity of our immune response.”

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