Florido, M.McColl, S.Appelberg, R.2010-03-262010-03-262009Immunobiology, 2009; 214(8):643-6520171-29851878-3279http://hdl.handle.net/2440/57069Copyright © 2009 Elsevier GmbH All rights reserved.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.enMycobacteriaT cellsCell-mediated immunityLungJournal article002009123910.1016/j.imbio.2008.12.0020002688456000012-s2.0-6765007711538481McColl, S. [0000-0003-0949-4660]