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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*

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

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.

Article first published online 11 September 2013Supplemental Digital Content is Available in the Text.

*Center of Excellence for Arthritis and Rheumatology, Louisiana State University Health Sciences Center, Shreveport, Louisiana;

Division of Gastroenterology and Hepatology, Department of Medicine, Louisiana State University Health Sciences Center, Shreveport, Louisiana; and

Department of Pathology, Louisiana State University Health Sciences Center, Shreveport, Louisiana.

Reprints: Dmitry V. Ostanin, PhD, Department of Medicine, Center of Excellence for Arthritis and Rheumatology, Louisiana State University Health Sciences Center, 1501 Kings Highway, P.O. Box 33932, Shreveport, LA 71130-3932 (e-mail:

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Web site (

D. V. Ostanin is supported by the CCFA Research Fellowship Grant (#1787) and the Arthritis Center of Excellence at LSU Health Sciences Center, and is supported by the Center of Excellence for Arthritis and Rheumatology funds and CCFA Career Developmental Award #2923. The remaining authors have no conflicts of interest to disclose.

Received May 23, 2013

Accepted August 11, 2013

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