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Genetic Differences in Bone Marrow-Derived Lymphoid Lineages Control Susceptibility to Experimental Autoimmune Myocarditis¹

Haiyan S. Li^2,*, Davinna L. Ligons^*, Noel R. Rose^2,*, and Mehmet L. Guler^*

^* Department of Pathology, and W. Harry Feinstone Department of Molecular Microbiology and Immunology, The Johns Hopkins University, Baltimore, MD 21205

Bone marrow (BM) transplantation has been used to study the cellular basis of genetic control of autoimmune diseases, but conclusions remain elusive due to the contradictory findings in different animal models. In the current study, we found that BM cells from myocarditis-susceptible A.SW mice can render irradiated, myocarditis-resistant B10.S recipient mice susceptible to myosin-induced myocarditis, indicating that hematopoietic cells express the genetic differences controlling susceptibility to autoimmune myocarditis. We then sought to differentiate the role of lymphoid vs nonlymphoid components of BM in the pathogenesis of myocarditis by comparing mixed chimeras receiving BM from A.SW wild-type or RAG^–/– mice mixed with BM from B10.S wild-type mice. This experiment clearly demonstrated that T and B lymphocytes were indispensable for transferring the susceptible phenotype to disease-resistant recipients. Our findings significantly narrow the cellular expression of genetic polymorphisms controlling the EAM phenotype.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work is supported by Research Grants R01 HL-077611 and R01 HL-067290 from the National Institutes of Health.

² Address correspondence and reprint requests to Dr. Noel R. Rose or Dr. Haiyan S. Li, Department of Pathology, Johns Hopkins University, 720 Rutland Avenue, Baltimore, MD 21205. E-mail addresses: nrrose{at}jhsph.edu or hli38{at}jhmi.edu

³ Abbreviations used in this paper: BM, bone marrow; EAM, experimental autoimmune myocarditis; CM, cardiac myosin; WT, wild type.