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|Title:||Delayed recruitment of lymphocytes into the lungs of CD30-deficient mice during aerogenic Mycobacterium avium infections|
|Citation:||Immunobiology, 2009; 214(8):643-652|
|Publisher:||Urban & Fischer Verlag|
|Manuela Flórido, Shaun R. McColl and Rui Appelberg|
|Abstract:||CD30 is a member of the tumor necrosis factor-receptor superfamily, a group of receptors known to act as accessory molecules in the development of the immune response. Control and CD30-deficient mice were aerogenically infected with Mycobacterium avium. Although the mycobacterial loads in the lungs were similar in both strains of mice, CD30-deficient animals exhibited delayed structuring of pulmonary granulomas and reduced recruitment of lymphocytes throughout a 240 days period of infection. Discrete alterations in the chemokine network were detected in the CD30-deficient animals although they showed no clear relation to the deficient inflammatory response. Thus CD30/CD153 interactions are involved in lung immune-mediated inflammation.|
|Keywords:||Mycobacteria; T cells; Cell-mediated immunity; Lung|
|Description:||Copyright © 2009 Elsevier GmbH All rights reserved.|
|Appears in Collections:||Molecular and Biomedical Science publications|
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