Deficient CCR7 signaling promotes T H2 polarization and B-cell activation in vivo

22Citations
Citations of this article
35Readers
Mendeley users who have this article in their library.

This article is free to access.

Abstract

The chemokine receptor CCR7 has a central role in regulating homing and positioning of T cells and DCs to lymph nodes (LNs) and participates in T-cell development and activation. In this study, we addressed the role of CCR7 signaling in T H2 polarization and B-cell activation. We provide evidence that the lack of CCR7 drives the capacity of naïve CD4 + T cells to polarize toward T H2 cells. This propensity contributes to a lymph node environment in CCR7-deficent mice characterized by increased expression of IL-4 and increased frequency of T H2 cells. We show that elevated IL-4 levels lead to B-cell activation characterized by up-regulated expression of MHC class II, CD23 and CD86. Activated B cells are in turn highly efficient in presenting antigen to CD4 + T cells and thus potentially contribute to the T H2 microenvironment. Taken together, our results support the idea of a CCR7-dependent patterning of T H2 responses, with absent CCR7 signaling favoring T H2 polarization, dislocation of T helper cells into the B-cell follicles and, as a consequence, B-cell activation. © 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

Cite

CITATION STYLE

APA

Moschovakis, G. L., Bubke, A., Dittrich-Breiholz, O., Braun, A., Prinz, I., Kremmer, E., & Förster, R. (2012). Deficient CCR7 signaling promotes T H2 polarization and B-cell activation in vivo. European Journal of Immunology, 42(1), 48–57. https://doi.org/10.1002/eji.201141753

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free