In recent years much attention has been focused on group of innate cells called innate lymphoid cells (ILCs). There are group 1 (TH1 behavior), group 2 (TH2 behavior) and group 3 (TH17 behavior) ILCs, so far.
This week, new paper in Nature Immunology from David Artis lab (extremely prolific research lab) showed that ILC2-specific arginase-1 (Arg1) contributes to lung allergic inflammation.
Arg1 is an enzyme that metabolizes the amino acid L-arginine. Most L-arginine metabolism occurs primarily in the liver, though immune cells can express it too during immune response (i.e. Arg1 activity is a key signature of alternatively activated macrophages). Here, fate-mapping study of Arg1-YFP-expressing cells in lungs of naive mice showed that Arg1 was mostly expressed by ILC2.
Papain challenge (TH2 trigger) induced expansion of Arg1+ lung ILC2.
Using genetic mouse model where Arg1 is selectively absent in ILC2, Arg1ΔILC, the authors showed that Arg1 deficiency impaired ILC2 expansion and allergic lung inflammation upon papain challenge.
Finally, the authors showed that lung allergic inflammation was not impaired if Arg1 was missing from macrophage lineage (Arg1ΔLyz2), implying dominant role of ILC2-derived Arg1 in papain induced lung allergic inflammation.
In summary, this study revealed ILC2-specific role of Arg1 in promoting type II immunity in response to TH2 triggers (papain and helminth parasite N. brasiliensis).
David Usharauli
This week, new paper in Nature Immunology from David Artis lab (extremely prolific research lab) showed that ILC2-specific arginase-1 (Arg1) contributes to lung allergic inflammation.
Arg1 is an enzyme that metabolizes the amino acid L-arginine. Most L-arginine metabolism occurs primarily in the liver, though immune cells can express it too during immune response (i.e. Arg1 activity is a key signature of alternatively activated macrophages). Here, fate-mapping study of Arg1-YFP-expressing cells in lungs of naive mice showed that Arg1 was mostly expressed by ILC2.
Papain challenge (TH2 trigger) induced expansion of Arg1+ lung ILC2.
Using genetic mouse model where Arg1 is selectively absent in ILC2, Arg1ΔILC, the authors showed that Arg1 deficiency impaired ILC2 expansion and allergic lung inflammation upon papain challenge.
Finally, the authors showed that lung allergic inflammation was not impaired if Arg1 was missing from macrophage lineage (Arg1ΔLyz2), implying dominant role of ILC2-derived Arg1 in papain induced lung allergic inflammation.
In summary, this study revealed ILC2-specific role of Arg1 in promoting type II immunity in response to TH2 triggers (papain and helminth parasite N. brasiliensis).
David Usharauli
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