Differential regulation of CCL21 in lymphoid/nonlymphoid tissues for effectively attracting T cells to peripheral tissues
J. Clin. Invest. James C. Lo, et al. 112:1495 doi:10.1172/JCI19188 [Go to this article.]

Figure 4
Airway inflammation induces the CCL21-Ser gene in an LT-dependent fashion. (a) LTβR signaling specifically induces CCL21-Ser. WT mice were injected i.p. with control or agonistic LTβR antibodies. RNA from the spleens and lungs were analyzed by real-time PCR for CCL21-Ser and CCL21-Leu. Each point reflects the fold induction in CCL21. (b) Spleen and lung cells respond to LTβR signals. Representative histograms of stromal cells from the spleen or lung stimulated with species control (black) or agonistic anti-LTβR (gray) antibody and stained with VCAM-1 antibody for analysis by flow cytometry is shown. (c) Airway inflammation induction of CCL21 in the lung is LT-dependent. WT or LTα^–/– mice were challenged with SEA and control or anti-LTβ antibodies were administered i.p. during the challenge phase only. Mice were killed 3 to 4 days after challenge and pulmonary CCL21 quantified as previously described (see Figure 3a). Student’s t tests were performed between naive and challenged, control challenged and anti-LTβ–challenged, and WT and LTα^–/– SEA-challenged groups and the resultant P values are shown. (d) Airway inflammation specifically induces the CCL21-Ser gene. Real-time PCR for the two CCL21 genes was performed on RNA extracted from lungs of naive and SEA-challenged WT and LTα^–/– mice. PCR reactions were performed in duplex with a GAPDH internal control for normalization. Columns and bars represent the mean ± SD.