| First Author | Flórido M | Year | 2009 |
| Journal | Immunobiology | Volume | 214 |
| Issue | 8 | Pages | 643-52 |
| PubMed ID | 19250702 | Mgi Jnum | J:309856 |
| Mgi Id | MGI:6708127 | Doi | 10.1016/j.imbio.2008.12.002 |
| Citation | Florido M, et al. (2009) Delayed recruitment of lymphocytes into the lungs of CD30-deficient mice during aerogenic Mycobacterium avium infections. Immunobiology 214(8):643-52 |
| abstractText | 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. |
