TLR4/MyD88-induced CD11b+ Gr-1 int F4/80+ non-migratory myeloid cells suppress Th2 effector function in the lung

M. Arora, S. L. Poe, T. B. Oriss, N. Krishnamoorthy, M. Yarlagadda, S. E. Wenzel, T. R. Billiar, A. Ray*, P. Ray

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

104 Scopus citations


In humans, environmental exposure to a high dose of lipopolysaccharide (LPS) protects from allergic asthma, the immunological underpinnings of which are not well understood. In mice, exposure to a high LPS dose blunted house dust mite-induced airway eosinophilia and T-helper 2 (Th2) cytokine production. Although adoptively transferred Th2 cells induced allergic airway inflammation in control mice, they were unable to do so in LPS-exposed mice. LPS promoted the development of a CD11b Gr1 int F4/80 lung-resident cell resembling myeloid-derived suppressor cells in a Toll-like receptor 4 and myeloid differentiation factor 88 (MyD88)-dependent manner that suppressed lung dendritic cell (DC)-mediated reactivation of primed Th2 cells. LPS effects switched from suppressive to stimulatory in MyD88 / mice. Suppression of Th2 effector function was reversed by anti-interleukin-10 (IL-10) or inhibition of arginase 1. Lineage neg bone marrow progenitor cells could be induced by LPS to develop into CD11b Gr1 int F4/80 cells both in vivo and in vitro that when adoptively transferred suppressed allergen-induced airway inflammation in recipient mice. These data suggest that CD11b Gr1 int F4/80 cells contribute to the protective effects of LPS in allergic asthma by tempering Th2 effector function in the tissue.

Original languageEnglish
Pages (from-to)578-593
Number of pages16
JournalMucosal Immunology
Issue number6
StatePublished - Nov 2010
Externally publishedYes


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