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Airway-specific recruitment of T cells is reduced in a CD26-deficient F344 rat substrain.

Abstract：

:Asthma is a chronic inflammatory disease affecting the airways. Increased levels of T cells are found in the lungs after the induction of an allergic-like inflammation in rats, and flow cytometry studies have shown that these levels are reduced in CD26-deficient rats. However, the precise anatomical sites where these newly recruited T cells appear primarily are unknown. Therefore, we quantified the distribution of T cells in lung parenchyma as well as in large, medium and small airways using immunohistochemical stainings combined with morphometric analyses. The number of T cells increased after the induction of an allergic-like inflammation. However, the differences between CD26-deficient and wild-type rats were not attributable to different cell numbers in the lung parenchyma, but the medium- and large-sized bronchi revealed significantly fewer T cells in CD26-deficient rats. These sites of T cell recruitment were screened further using immunohistochemistry and quantitative real-time polymerase chain reaction with regard to two hypotheses: (i) involvement of the nervous system or (ii) expression of chemokines with properties of a T cell attractor. No topographical association was found between nerves and T cells, but a differential transcription of chemokines was revealed in bronchi and parenchyma. Thus, the site-specific recruitment of T cells appears to be a process mediated by chemokines rather than nerve-T cell interactions. In conclusion, this is the first report showing a differential site-specific recruitment of T cells to the bronchi in a CD26-deficient rat substrain during an asthma-like inflammation.

journal_name

Clin Exp Immunol

journal_title

Clinical and experimental immunology

authors

Schade J,Schmiedl A,Kehlen A,Veres TZ,Stephan M,Pabst R,von Hörsten S

doi

10.1111/j.1365-2249.2009.03991.x

subject

Has Abstract

pub_date

2009-10-01 00:00:00

pages

133-42

issue

1

eissn

0009-9104

issn

1365-2249

pii

CEI3991

journal_volume

158

pub_type

杂志文章

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