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Infection and Immunity, October 1998, p. 4994-5000, Vol. 66, No. 10
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Interleukin-12 Is Essential for a Protective Th1 Response in Mice Infected with Cryptococcus neoformans

Klaus Decken,1,dagger Gabriele Köhler,2 Kathrin Palmer-Lehmann,1 Andrea Wunderlin,1 Frank Mattner,1,Dagger Jeanne Magram,3,§ Maurice K. Gately,3 and Gottfried Alber1,*

Department of Infectious Diseases, F. Hoffmann-La Roche AG, Basel, Switzerland1; Department of Pathology, Albert Ludwig University, Freiburg, Germany2; and Department of Inflammation/ Autoimmune Diseases, Hoffmann-La Roche Inc., Nutley, New Jersey3

Received 20 March 1998/Returned for modification 2 July 1998/Accepted 21 July 1998

To analyze the roles of interleukin-12 (IL-12) and the IL-12-dependent Th1 response in resistance to Cryptococcus neoformans, we have established a chronic infection model in wild-type mice and in mice with targeted disruptions of the genes for the IL-12p35 and IL-12p40 subunits (IL-12p35-/- and IL-12p40-/- mice, respectively) as well as in mice with a targeted disruption of the IL-4 gene. Long-term application of exogenous IL-12 prevented death of infected wild-type mice for the entire period of the experiment (up to 180 days) but did not resolve the infection. Infected IL-12p35-/- and IL-12p40-/- mice died significantly earlier than infected wild-type mice, whereas infection of IL-4-deficient mice led to prolonged survival. Interestingly, infected IL-12p40-/- mice died earlier and developed higher organ burdens than IL-12p35-/- mice, which, for the first time in an infection model, suggests a protective role of the IL-12p40 subunit independent of the IL-12 heterodimer. The fungal organ burdens of IL-4-deficient mice and IL-12-treated wild-type mice were significantly reduced compared to those of untreated wild-type mice and IL-12-deficient mice. Histopathological analysis revealed reduction of the number of granulomatous lesions following treatment with IL-12. Susceptibility of both IL-12p35-/- and IL-12p40-/- mice was associated with marginal production of gamma interferon and elevated levels of IL-4 from CD4+ T cells, which indicates Th2 polarization in the absence of IL-12, whereas wild-type mice developed a Th1 response. Taken together, our data emphasize the essential role of IL-12 for protective Th1 responses against C. neoformans.

* Corresponding author. Present address: Immunology Unit, Faculty of Veterinary Medicine, University of Leipzig, Zwickauer Straße 53, D-04103 Leipzig, Germany. Phone: (49) 341 97 38 328. Fax: (49) 341 97 38 147. E-mail: alber{at}rz.uni-leipzig.de.

dagger Present address: Immunology Unit, Faculty of Veterinary Medicine, University of Leipzig, Leipzig, Germany.

Dagger Present address: Roche Milano Ricerche, Milan, Italy.

§ Present address: Cadus Pharmaceutical Corporation, Tarrytown, N.Y.

Infection and Immunity, October 1998, p. 4994-5000, Vol. 66, No. 10
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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