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Mucosal T lymphocyte numbers are selectively reduced in integrin α(E) (CD103)-deficient mice

Schön, Michael P. ; Arya, Anu ; Murphy, Elizabeth A. LU ; Adams, Cassandra M. ; Strauch, Ulrike G. ; Agace, William W. LU ; Marsal, Jan LU ; Donohue, John P. ; Her, Helen and Beier, David R. , et al. (1999) In Journal of Immunology 162(11). p.6641-6649
Abstract

The mucosal lymphocyte integrin α(E)(CD103)β7 is thought to be important for intraepithelial lymphocyte (IEL) localization or function. We cloned the murine integrin gene encoding α(E), localized it to chromosome 11, and generated integrin α(E)-deficient mice. In α(E)(-/-) mice, intestinal and vaginal IEL numbers were reduced, consistent with the known binding of α(E)β7, to E-cadherin expressed on epithelial cells. However, it was surprising that lamina propria T lymphocyte numbers were diminished, as E-cadherin is not expressed in the lamina propria. In contrast, peribronchial, intrapulmonary, Peyer's patch, and splenic T lymphocyte numbers were not reduced in α(E)-deficient mice. Thus, α(E)β7 was... (More)

The mucosal lymphocyte integrin α(E)(CD103)β7 is thought to be important for intraepithelial lymphocyte (IEL) localization or function. We cloned the murine integrin gene encoding α(E), localized it to chromosome 11, and generated integrin α(E)-deficient mice. In α(E)(-/-) mice, intestinal and vaginal IEL numbers were reduced, consistent with the known binding of α(E)β7, to E-cadherin expressed on epithelial cells. However, it was surprising that lamina propria T lymphocyte numbers were diminished, as E-cadherin is not expressed in the lamina propria. In contrast, peribronchial, intrapulmonary, Peyer's patch, and splenic T lymphocyte numbers were not reduced in α(E)-deficient mice. Thus, α(E)β7 was important for generating or maintaining the gut and vaginal T lymphocytes located diffusely within the epithelium or lamina propria but not for generating the gut-associated organized lymphoid tissues. Finally, the impact of α(E) deficiency upon intestinal IEL numbers was greater at 3-4 wk of life than in younger animals, and affected the TCR αβ+ CD8+ T cells more than the γδ T cells or the TCR αβ+ CD4+CD8- population. These findings suggest that α(E)β7 is involved in the expansion/recruitment of TCR αβ+ CD8+ IEL following microbial colonization. Integrin α(E)-deficient mice will provide an important tool for studying the role of α(E)β7 and of α(E)β7-expressing mucosal T lymphocytes in vivo.

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publishing date
type
Contribution to journal
publication status
published
in
Journal of Immunology
volume
162
issue
11
pages
9 pages
publisher
American Association of Immunologists
external identifiers
  • pmid:10352281
  • scopus:0033151953
ISSN
0022-1767
language
English
LU publication?
no
id
b6f60d4f-b4b7-4e88-a4ad-56e93ba7b010
alternative location
http://www.jimmunol.org/content/162/11/6641
date added to LUP
2019-05-30 13:51:03
date last changed
2024-06-25 16:52:13
@article{b6f60d4f-b4b7-4e88-a4ad-56e93ba7b010,
  abstract     = {{<p>The mucosal lymphocyte integrin α(E)(CD103)β<sub>7</sub> is thought to be important for intraepithelial lymphocyte (IEL) localization or function. We cloned the murine integrin gene encoding α(E), localized it to chromosome 11, and generated integrin α(E)-deficient mice. In α(E)(-/-) mice, intestinal and vaginal IEL numbers were reduced, consistent with the known binding of α(E)β<sub>7</sub>, to E-cadherin expressed on epithelial cells. However, it was surprising that lamina propria T lymphocyte numbers were diminished, as E-cadherin is not expressed in the lamina propria. In contrast, peribronchial, intrapulmonary, Peyer's patch, and splenic T lymphocyte numbers were not reduced in α(E)-deficient mice. Thus, α(E)β<sub>7</sub> was important for generating or maintaining the gut and vaginal T lymphocytes located diffusely within the epithelium or lamina propria but not for generating the gut-associated organized lymphoid tissues. Finally, the impact of α(E) deficiency upon intestinal IEL numbers was greater at 3-4 wk of life than in younger animals, and affected the TCR αβ<sup>+</sup> CD8<sup>+</sup> T cells more than the γδ T cells or the TCR αβ<sup>+</sup> CD4<sup>+</sup>CD8<sup>-</sup> population. These findings suggest that α(E)β<sub>7</sub> is involved in the expansion/recruitment of TCR αβ<sup>+</sup> CD8<sup>+</sup> IEL following microbial colonization. Integrin α(E)-deficient mice will provide an important tool for studying the role of α(E)β<sub>7</sub> and of α(E)β<sub>7</sub>-expressing mucosal T lymphocytes in vivo.</p>}},
  author       = {{Schön, Michael P. and Arya, Anu and Murphy, Elizabeth A. and Adams, Cassandra M. and Strauch, Ulrike G. and Agace, William W. and Marsal, Jan and Donohue, John P. and Her, Helen and Beier, David R. and Olson, Sara and Lefrancois, Leo and Brenner, Michael B. and Grusby, Michael J. and Parker, Christina M.}},
  issn         = {{0022-1767}},
  language     = {{eng}},
  month        = {{06}},
  number       = {{11}},
  pages        = {{6641--6649}},
  publisher    = {{American Association of Immunologists}},
  series       = {{Journal of Immunology}},
  title        = {{Mucosal T lymphocyte numbers are selectively reduced in integrin α(E) (CD103)-deficient mice}},
  url          = {{http://www.jimmunol.org/content/162/11/6641}},
  volume       = {{162}},
  year         = {{1999}},
}