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

Florido, M.; McColl, S.; Appelberg, R.

doi:10.1016/j.imbio.2008.12.002

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

Date

2009

Authors

Florido, M.

McColl, S.

Appelberg, R.

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Journal article

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Immunobiology, 2009; 214(8):643-652

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Manuela Flórido, Shaun R. McColl and Rui Appelberg

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10.1016/j.imbio.2008.12.002

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.

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https://doi.org/10.1016/j.imbio.2008.12.002

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http://hdl.handle.net/2440/57069

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

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