Delayed recruitment of lymphocytes into the lungs of CD30-deficient mice during aerogenic Mycobacterium avium infections.
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.
Flórido
Manuela
M
Laboratory of Microbiology and Immunology of Infection, Instituto de Biologia Molecular e Celular (IBMC), University of Porto, Rua do Campo Alegre 823, 4150-180 Porto, Portugal.
McColl
Shaun R
SR
Appelberg
Rui
R
D000818:Animals; D002465:Cell Movement / Q000235:genetics / Q000276:immunology; D002478:Cells, Cultured; D018925:Chemokines; D005260:Female; D015769:Granuloma, Respiratory Tract / Q000276:immunology / Q000382:microbiology / Q000503:physiopathology; D017730:Ki-1 Antigen / Q000172:deficiency* / Q000235:genetics / Q000276:immunology; D008168:Lung / Q000382:microbiology / Q000473:pathology*; D008213:Lymphocyte Activation / Q000235:genetics; D008214:Lymphocytes / Q000276:immunology / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009162:Mycobacterium avium / Q000254:growth & development / Q000276:immunology* / Q000472:pathogenicity; D014397:Tuberculosis, Pulmonary / Q000276:immunology* / Q000382:microbiology / Q000473:pathology / Q000503:physiopathology; D014774:Virulence
D018925:Chemokines; D017730:Ki-1 Antigen