by promoting Toll-like receptor-dependent CD1a-reactive T cell responses to endogenous ligands. These findings define a previously unrecognized role for ILC2 in lipid surveillance and identify shared pathways of CD1a- and PLA2G4A-dependent ILC2 inflammation amenable to therapeutic intervention.
No takes yet. Share an insight, caveat, or question.
Hardman et al. (2017) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: