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Macrophages, CD4⁺ or CD8⁺ Cells Are Each Sufficient for Protection against Chlamydia pneumoniae Infection through their Ability to Secrete IFN-¹

Antonio Gigliotti Rothfuchs^2,*, Maria Regina Kreuger^2,, Hans Wigzell^* and Martin E. Rottenberg^3,*

^* Microbiology and Tumorbiology Center, Karolinska Institute, Stockholm, Sweden; and Centro de Ciências da Saúde, Universidade do Vale do Itajai, Itajai, Brasil

By using a T, B, or NK cell-deficient mouse strain (recombinase-activating gene (RAG)-1^-/-/common cytokine receptor -chain (_CR)), and T and B cell and IFN--deficient (RAG-1^-/-/IFN-^-/-) mice, we have studied the generation of immunity against infection by Chlamydia pneumoniae. We found that IFN- secreted by innate-cell populations protect against C. pneumoniae infection. However, NK cells were not needed for such IFN--dependent innate immune protection. Inoculation of wild type, but not IFN-^-/- bone marrow-derived macrophages protected RAG-1^-/-/IFN-^-/- mice against C. pneumoniae infection. In line, pulmonary macrophages from RAG-1^-/- C. pneumoniae-infected mice expressed IFN- mRNA. Reconstitution of RAG-1^-/-/_cR^-/- or RAG-1^-/-/IFN-^-/- mice with CD4⁺ or CD8⁺ cells by i.v. transfer of FACS sorted wild type spleen cells (SC) increased resistance to C. pneumoniae infection. On the contrary, no protection was observed upon transfer of IFN-^-/- CD4⁺ or IFN-^-/- CD8⁺ SC. T cell-dependent protection against C. pneumoniae was weaker when IFN-R^-/- CD4⁺ or IFN-R^-/- CD8⁺ SC were inoculated into RAG-1^-/-/IFN-^-/- mice. Thus both nonlymphoid and T cell-derived IFN- can play a central and complementary role in protection against C. pneumoniae. IFN- secreted by nonlymphoid cells was not required for T cell-mediated protection against C. pneumoniae; however, IFN- regulated T cell protective functions.

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