Induction and effector phase of allergic lung inflammation is independent of CCL21/CCL19 and LT-beta

The chemokines CCL21 and CCL19, and cell bound TNF family ligand lymphotoxin beta (LTbeta), 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 LTbet...

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Bibliographic Details
Published in:International journal of medical sciences 2009-01, Vol.6 (2), p.85-92
Main Authors: Ploix, Corinne, Zuberi, Riaz I, Liu, Fu-Tong, Carson, Monica J, Lo, David D
Format: Article
Language:English
Subjects:
Animals
Chemokine CCL19 - deficiency
Chemokine CCL19 - genetics
Chemokine CCL21 - deficiency
Chemokine CCL21 - genetics
Crosses, Genetic
Lymphotoxin-beta - deficiency
Lymphotoxin-beta - genetics
Mice
Mice, Inbred BALB C
Mice, Knockout
Mice, Mutant Strains
Ovalbumin - immunology
Pneumonia - immunology
Pneumonia - metabolism
Pneumonia - pathology
Research Paper
Respiratory Hypersensitivity - immunology
Respiratory Hypersensitivity - metabolism
Respiratory Hypersensitivity - pathology
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Summary:The chemokines CCL21 and CCL19, and cell bound TNF family ligand lymphotoxin beta (LTbeta), 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 LTbeta 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 LTbeta 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 LTbeta.
ISSN:1449-1907
1449-1907
DOI:10.7150/ijms.6.85