Chlamydia trachomatis pneumonia in the severe combined immunodeficiency (SCID) mouse

D. M. Magee, J. U. Igietseme, J. G. Smith, C. A. Bleicker, B. G. Grubbs, J. Schachter, R. G. Rank, D. M. Williams

Research output: Contribution to journalArticlepeer-review

24 Scopus citations


We have developed a model of pneumonia caused by the mouse pneumonitis agent (MoPn, murine Chlamydia trachomatis) in the C.B-17 severe combined immunodeficiency (SCID) mouse. In contrast to our prior models in the nude athymic (nu/nu) and heterozygous (nu/+) mouse, SCID mice lack B-cell function and γδ T-cell function. SCID mice were more susceptible to MoPn than nu/nu or nu/+ mice both by criteria of mortality and quantitative lung culture. SCID mice could be reconstituted with thymocytes to be more resistant to MoPn (in the absence of significant antibody production), but the protection was modest and less than that in T-cell reconstituted nu/nu mice in our previous studies. A nu/+ MoPn-specific T-cell clone with a Th1-like cytokine profile also provided modest but significant protection without significant antibody production. The SCID mouse is a useful model to study T-cell-mediated immunity to MoPn in a B cell and γδ T-cell-deficient environment.

Original languageEnglish (US)
Pages (from-to)305-311
Number of pages7
JournalRegional Immunology
Issue number6
StatePublished - 1993
Externally publishedYes

ASJC Scopus subject areas

  • Immunology


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