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Inflammatory Bowel Diseases:
doi: 10.1097/MIB.0b013e3182a8df0a
Original Basic Science Articles

Roles of T cell–Associated L-selectin and β7 Integrins During Induction and Regulation of Chronic Colitis

Kurmaeva, Elvira MS*; Boktor, Moheb MD; Zhang, Songling MD; Bao, Richard MD; Berney, Seth MD*; Ostanin, Dmitry V. PhD*

Supplemental Author Material
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Abstract

Background:

L-selectin (CD62L) and β7 integrins are important for trafficking of naive T cells under steady-state conditions. The objectives of this study were to dissect the requirements for T cell–associated CD62L and β7 integrins during initiation, progression, and regulation of chronic colitis.

Methods:

Using the T-cell transfer model, we compared colitogenic potential between T cells lacking one or both of these molecules with wild-type T cells. To assess trafficking of cells to the secondary lymphoid tissue and the gut, we performed co-homing experiments.

Results:

Adoptive transfer of wild-type, CD62L−/− or β7−/− single-deficient T cells induced moderate to severe disease with slightly different kinetics. However, transfer of CD62L−/− β7−/− double-deficient (DKO) T cells produced significantly attenuated gut inflammation, which correlated with fewer T cells and reduced levels of proinflammatory cytokines in the colon lamina propria. Our subsequent experiments established that lack of colitogenic potential of these cells was due to inability of DKO T cells to home to the secondary lymphoid tissue. Furthermore, homing of in vitro–generated effector DKO T cells to the inflamed intestine was significantly impaired. Lastly, DKO regulatory T cells were ineffective at suppressing colitis induced by wild-type T cells.

Conclusions:

We established that T cells can use either CD62L or β7 integrins to induce chronic colitis, but lack of both abrogates their colitogenic potential. Effector T cells critically rely on β7 integrin during their recruitment to the inflamed intestinal mucosa. Finally, regulation of intestinal inflammation by regulatory T cells requires one or both of these adhesion molecules.

Copyright © 2013 Crohn's & Colitis Foundation of America, Inc.

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