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

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 r...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2008-06, Vol.180 (11), p.7480-7484
Main Authors: Li, Haiyan S, Ligons, Davinna L, Rose, Noel R, Guler, Mehmet L
Format: Article
Language:English
Subjects:
Animals
Autoimmune Diseases - chemically induced
Autoimmune Diseases - genetics
Autoimmune Diseases - immunology
Bone Marrow Cells - immunology
Bone Marrow Transplantation - immunology
Cardiac Myosins - immunology
Cardiac Myosins - pharmacology
Cell Lineage
Genetic Predisposition to Disease
Lymphocytes - immunology
Mice
Mice, Mutant Strains
Myocarditis - chemically induced
Myocarditis - genetics
Myocarditis - immunology
Myocardium - cytology
Myocardium - immunology
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Summary: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.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.180.11.7480