The IL-6R α chain controls lung CD4⁺CD25⁺ Treg development and function during allergic airway inflammation in vivo
J. Clin. Invest. Aysefa Doganci, et al. 115:313 doi:10.1172/JCI22433 [Go to this article.]

Figure 7
Increased number and augmented immunosuppressive function of CD4⁺CD25⁺ T cells in the lungs of anti–IL-6R–treated, OVA-sensitized mice. (A) i.n. but not i.p. anti–IL-6R antibody treatment after OVA sensitization and challenge led to an induction of CD4⁺CD25⁺ T cell number in the lung (*P = 0.057). (B) IL-6 levels were increased in BALF of OVA-sensitized mice as compared to those of saline-treated mice. i.p. but not i.n. injection of anti–IL-6R antibodies led to a further increase of IL-6 in the airways. (C) CD4⁺CD25⁺ T cells isolated from the lungs of anti–IL-6R antibody–treated (i.n.) mice inhibited proliferation of CFSE-labeled target CD4⁺ spleen T cells more efficiently compared to CD4⁺CD25⁺ T cells isolated from the lungs of OVA-sensitized and -challenged, untreated mice. Mean values ± SEM; n = 5 mice per group; *P < 0.05. (D) Histograms of a representative cell population of CD4⁺ spleen cells labeled with CFSE and coincubated for 4 days with either CD4⁺CD25⁺ or CD4⁺CD25^– cells isolated from the lungs of different groups. Percentages indicate the number of spleen CD4⁺/CFSE-labeled cells at day 4 (M1, 20 hours). (E) RT-PCR for the IL-6R α chain shows selective expression on Foxp3⁺ CD4⁺CD25⁺ lung T cells but not CD4⁺CD25^– lung T cells. One representative experiment out of 3 is shown. (F) phospho–STAT-3 (pSTAT3) immunostaining in CD4⁺CD25⁺ cells. Spleen CD4⁺CD25⁺ T cells were incubated either with medium alone (left panel), with 20 ng/ml of IL-6 (middle panel), or with IL-6 (20 ng/ml) and anti–IL-6R antibodies (10 μg/ml) (right panel). Magnification, ×200.