Effector T Cell Egress via Afferent Lymph Modulates Local Tissue Inflammation.

Journal Article (Journal Article)

Memory/effector T cells recirculate through extralymphoid tissues by entering from blood and egressing via afferent lymph. Although T cell entry into effector sites is key to inflammation, the relevance of T cell egress to this process is unknown. In this study, we found that Ag recognition at the effector site reduced the tissue egress of proinflammatory Th1 cells in a mouse model of delayed hypersensitivity. Transgenic expression of "tissue exit receptor" CCR7 enhanced lymphatic egress of Ag-sequestered Th1 cells from the inflamed site and alleviated inflammation. In contrast, lack of CCR7 on Th1 cells diminished their tissue egress while enhancing inflammation. Lymph-borne Th1 and Th17 cells draining the inflamed skin of sheep migrated toward the CCR7 ligand CCL21, suggesting the CCR7-CCL21 axis as a physiological target in regulating inflammation. In conclusion, exit receptors can be targeted to modulate T cell dwell time and inflammation at effector sites, revealing T cell tissue egress as a novel control point of inflammation.

Full Text

Duke Authors

Cited Authors

  • Gómez, D; Diehl, MC; Crosby, EJ; Weinkopff, T; Debes, GF

Published Date

  • October 15, 2015

Published In

Volume / Issue

  • 195 / 8

Start / End Page

  • 3531 - 3536

PubMed ID

  • 26355150

Pubmed Central ID

  • PMC4571282

Electronic International Standard Serial Number (EISSN)

  • 1550-6606

Digital Object Identifier (DOI)

  • 10.4049/jimmunol.1500626


  • eng

Conference Location

  • United States