Induction and effector phase of allergic lung inflammation is independent of CCL21/CCL19 and LT-beta
<p>The chemokines CCL21 and CCL19, and cell bound TNF family ligand lymphotoxin beta (LTβ), have been associated with numerous chronic inflammatory diseases. A general role in chronic inflammatory diseases cannot be assumed however; in the case of allergic inflammatory disease, CCL21/...
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| Format: | Article |
| Language: | English |
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Ivyspring International Publisher
2009-01-01
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| Series: | International Journal of Medical Sciences |
| Online Access: | http://www.medsci.org/v06p0085.htm |
| _version_ | 1811235017478635520 |
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| author | Corinne Ploix, Riaz I. Zuberi, Fu-Tong Liu, Monica J. Carson, David D. Lo |
| author_facet | Corinne Ploix, Riaz I. Zuberi, Fu-Tong Liu, Monica J. Carson, David D. Lo |
| author_sort | Corinne Ploix, Riaz I. Zuberi, Fu-Tong Liu, Monica J. Carson, David D. Lo |
| collection | DOAJ |
| description | <p>The chemokines CCL21 and CCL19, and cell bound TNF family ligand lymphotoxin beta (LTβ), have been associated with numerous chronic inflammatory diseases. A general role in chronic inflammatory diseases cannot be assumed however; in the case of allergic inflammatory disease, CCL21/CCL19 and LTβ have not been associated with the induction, recruitment, or effector function of Th2 cells nor dendritic cells to the lung. We have examined the induction of allergic inflammatory lung disease in mice deficient in CCL21/CCL19 or LTβ and found that both kinds of mice can develop allergic lung inflammation. To control for effects of priming differences in knockout mice, adoptive transfers of Th2 cells were also performed, and they showed that such effector cells had equivalent effects on airway hyper-responsiveness in both knockout background recipients. Moreover, class II positive antigen presenting cells (B cells and CD11c+ dendritic cells) showed normal recruitment to the peribronchial spaces along with CD4 T cells. Thus, the induction of allergic responses and recruitment of both effector Th2 cells and antigen presenting cells to lung peribronchial spaces can develop independently of CCL21/CCL19 and LTβ.</p> |
| first_indexed | 2024-04-12T11:45:09Z |
| format | Article |
| id | doaj.art-7e989fb1044d4ede8d8bb3f6889fe306 |
| institution | Directory Open Access Journal |
| issn | 1449-1907 |
| language | English |
| last_indexed | 2024-04-12T11:45:09Z |
| publishDate | 2009-01-01 |
| publisher | Ivyspring International Publisher |
| record_format | Article |
| series | International Journal of Medical Sciences |
| spelling | doaj.art-7e989fb1044d4ede8d8bb3f6889fe3062022-12-22T03:34:24ZengIvyspring International PublisherInternational Journal of Medical Sciences1449-19072009-01-01628592Induction and effector phase of allergic lung inflammation is independent of CCL21/CCL19 and LT-betaCorinne Ploix, Riaz I. Zuberi, Fu-Tong Liu, Monica J. Carson, David D. Lo<p>The chemokines CCL21 and CCL19, and cell bound TNF family ligand lymphotoxin beta (LTβ), have been associated with numerous chronic inflammatory diseases. A general role in chronic inflammatory diseases cannot be assumed however; in the case of allergic inflammatory disease, CCL21/CCL19 and LTβ have not been associated with the induction, recruitment, or effector function of Th2 cells nor dendritic cells to the lung. We have examined the induction of allergic inflammatory lung disease in mice deficient in CCL21/CCL19 or LTβ and found that both kinds of mice can develop allergic lung inflammation. To control for effects of priming differences in knockout mice, adoptive transfers of Th2 cells were also performed, and they showed that such effector cells had equivalent effects on airway hyper-responsiveness in both knockout background recipients. Moreover, class II positive antigen presenting cells (B cells and CD11c+ dendritic cells) showed normal recruitment to the peribronchial spaces along with CD4 T cells. Thus, the induction of allergic responses and recruitment of both effector Th2 cells and antigen presenting cells to lung peribronchial spaces can develop independently of CCL21/CCL19 and LTβ.</p>http://www.medsci.org/v06p0085.htm |
| spellingShingle | Corinne Ploix, Riaz I. Zuberi, Fu-Tong Liu, Monica J. Carson, David D. Lo Induction and effector phase of allergic lung inflammation is independent of CCL21/CCL19 and LT-beta International Journal of Medical Sciences |
| title | Induction and effector phase of allergic lung inflammation is independent of CCL21/CCL19 and LT-beta |
| title_full | Induction and effector phase of allergic lung inflammation is independent of CCL21/CCL19 and LT-beta |
| title_fullStr | Induction and effector phase of allergic lung inflammation is independent of CCL21/CCL19 and LT-beta |
| title_full_unstemmed | Induction and effector phase of allergic lung inflammation is independent of CCL21/CCL19 and LT-beta |
| title_short | Induction and effector phase of allergic lung inflammation is independent of CCL21/CCL19 and LT-beta |
| title_sort | induction and effector phase of allergic lung inflammation is independent of ccl21 ccl19 and lt beta |
| url | http://www.medsci.org/v06p0085.htm |
| work_keys_str_mv | AT corinneploixriazizuberifutongliumonicajcarsondaviddlo inductionandeffectorphaseofallergiclunginflammationisindependentofccl21ccl19andltbeta |