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. Author manuscript; available in PMC: 2012 May 1.
Published in final edited form as: Nat Immunol. 2011 Nov;12(11):1045–1054. doi: 10.1031/ni.2131

Figure 2. Development of lung ILCs requires Id2 but is independent of microbial signals.

Figure 2

(a,c) mRNA expression of Id2 (a) or RORc (c) in sort purified Lin− CD90+ CD25+ lung ILCs and Lin− CD90+ CD4+ splenic LTi cells, normalized to β-actin and shown relative to expression levels in purified B220+ B cells. n = 3 replicates, each replicate consisting of spleens (LTi cells) or lungs (ILCs) pooled from 5 C57BL/6 WT mice. (b) Flow cytometry plots of CD90+ CD25+ lung ILCs in WT or Id2-deficient bone marrow chimeras sacrificed 10 weeks post reconstitution, gated on live Lin− donor cells. Data is representative of 3 experiments, n = 2–4 Id2+/+ or Id2−/− chimeras. (d) Flow cytometry plot of RORγt expression in CD90+ CD25+ lung ILCs (dashed black line) or CD90+ CD4+ LTi cells (solid black line) compared to isotype antibody control (gray shaded). (e) Representative flow cytometry plots, total frequency, and absolute cell number of lung Lin− CD90+ CD25+ ILCs in conventional C57BL/6 (CNV) or germ-free (GF) mice. (f) Cell surface expression of c-kit, CD127, and T1-ST2 on Lin− CD90+ CD25+ lung ILCs in CNV (solid black line) or GF (dashed black line) mice compared to isotype controls (gray shaded). (e-f) Data is representative of 2 independent experiments. Data shown are the mean ± SEM, n = 3–5 CNV or GF mice.