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   <subfield code="a">Genes outside the major histocompatibility complex control resistance and susceptibility to experimental Lyme arthritis</subfield>
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   <subfield code="c">[Charles R. Brown, Steven L. Reiner]</subfield>
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   <subfield code="a">The mechanism controlling the development of experimental Lyme arthritis remains poorly understood. Mice with the H-2k haplotype have generally been thought to be more susceptible to Lyme arthritis development than those with the H-2d haplotype. In the present study the role of genes within the major histocompatibility complex (MHC) in determining resistance or susceptibility to the development of experimental Lyme arthritis was investigated. We found that C3H congenic mice were equally susceptible, and DBA congenic mice equally resistant, to arthritis development regardless of their H-2 haplotype (H-2k or H-2d). These results indicate that genes outside the murine MHC are the major determinants of both resistance and susceptibility to the development of experimental Lyme arthritis.</subfield>
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   <subfield code="a">Key wordsBorrelia burgdorferi</subfield>
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   <subfield code="a">Lyme borreliosis</subfield>
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   <subfield code="a">MHC restriction</subfield>
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   <subfield code="a">Arthritis</subfield>
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   <subfield code="a">Metadata rights reserved</subfield>
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