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Brief Definitive Reports

Shuo Li^*, Christian Kurts, Frank Köntgen, Stephen R. Holdsworth^*, and Peter G. Tipping^*

From the ^* Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, Clayton, 3168, Victoria, Australia; and the Immunology Division, Walter and Eliza Hall Institute, Parkville, 3050, Victoria, Australia

The requirement for major histocompatibility complex class II (MHC II) to initiate immune renal injury was studied in a murine model of CD4⁺ T cell–dependent crescentic glomerulonephritis (GN). C57BL/6 (MHC II^+/+) mice developed crescentic GN with glomerular CD4⁺ T cell infiltration and renal injury, in response to a nephritogenic antigen (sheep globulin) planted on their glomerular basement membrane. MHC II–deficient C57BL/6 mice (MHC II^–/–) did not develop crescentic GN, CD4⁺ T cell infiltration, or injury, indicating that this form of immune glomerular injury is MHC II dependent. The requirement for MHC II expression by intrinsic renal cells was studied in chimeric mice, which expressed MHC II on bone marrow–derived cells and in the thymus, but not in the kidneys. These chimeric mice had normal T and B cell populations and MHC II expression in their spleens and lymph nodes and developed an immune response to systemically and cutaneously administered sheep globulin. However, they did not develop crescentic GN, CD4⁺ T cell infiltration, or renal injury in response to the sheep globulin planted in their glomeruli. These studies demonstrate that interaction of CD4⁺ T cells with intrinsic renal cells expressing MHC II is required for development of cell-mediated immune renal injury.

Key Words: major histocompatibility complex • glomerulonephritis • T lymphocyte • kidney • mice

The technical help of Mr. P. Hutchinson and Ms. J. Tsoupas is gratefully acknowledged. We thank William Heath, Dianne Mathis, and Christophe Benoit for valuable discussions.

C. Kurts's current address is Department of Nephrology, Medizinische Hochschule, 30625, Hannover, Germany. E-mail: ckurts{at}compuserve.com

S. Li and C. Kurts contributed equally to this paper.

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