Delayed recruitment of lymphocytes into the lungs of CD30-deficient mice during aerogenic Mycobacterium avium infections

• Type: Article in International Scientific Journal
• Date: 2009

Authors

Manuela Florido (Author) Other; Shaun R McColl (Author) Other; Rui Appelberg (Author) ICBAS

Journal

Title: Immunobiology

Vol. 214

Pages: 643-652

ISSN: 0171-2985

Publisher: Elsevier

Indexing

ISI Web of Knowledge - 1 Citation

Scopus - 1 Citation

Pubmed / Medline

Scientific classification

FOS: Medical and Health sciences > Basic medicine

CORDIS: Health sciences > Medical sciences > Medicine > Infections

Other information

Authenticus ID: P-00H-APD

DOI: 10.1016/j.imbio.2008.12.002

Abstract (EN): 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/CD 153 interactions are involved in lung immune-mediated inflammation.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 10