Abstract
Innate lymphoid cells (ILC) are important players of early immune defenses in situations like lymphoid organogenesis or in case of immune response to inflammation, infection and cancer. Th1 and Th2 antagonism is crucial for the regulation of immune responses, however mechanisms are still unclear for ILC functions. ILC2 and NK cells were reported to be both involved in allergic airway diseases and were shown to be able to interplay in the regulation of the immune response. CXCR6 is a common chemokine receptor expressed by all ILC, and its deficiency affects ILC2 and ILC1/NK cell numbers and functions in lungs in both steady-state and inflammatory conditions. We determined that the absence of a specific ILC2 KLRG1+ST2− subset in CXCR6-deficient mice is probably dependent on CXCR6 for its recruitment to the lung under inflammation. We show that despite their decreased numbers, lung CXCR6-deficient ILC2 are even more activated cells producing large amount of type 2 cytokines that could drive eosinophilia. This is strongly associated to the decrease of the lung Th1 response in CXCR6-deficient mice.
Highlights
Innate lymphoid cells (ILC) are lymphocytes that do not express rearranged antigen receptors such as T and B cells
We examined the proportion of lung ILC subsets that express the chemokine receptor CXCR6 in homeostatic conditions using Rag2−/− CXCR6 reporter mice (Rag2−/− CXCR6+/GFP)
We assessed the effect of CXCR6 deficiency on lung ILC2 and NK/ILC1 in steady state and after papain-driven inflammation into the lungs
Summary
Innate lymphoid cells (ILC) are lymphocytes that do not express rearranged antigen receptors such as T and B cells. Considered as tissue-resident cells, they contribute to the maintenance of tissue homeostasis and the containment of commensals by cytokine production at mucosal barriers They are critical during immune responses to pathogens with a concomitant action on tissue inflammation. Lung ILC2 play a crucial role in promoting allergic airway inflammation during innate immune responses [2,3], whereas lung NK cells could regulate the early type 2 immune response by an IFNγ retro-control [4]. NK cells can protect from OVA-induced asthma by contributing to the resolution of allergic lung inflammation in mice. They were shown as potent cytotoxic cells against eosinophils and specific CD4+ T cells [10]. Models of contact hypersensitivity have suggested that ILC2 are potent Th1 negative regulators for type 1 immune responses [13]
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