XXXX : mediation by complex immune events.

@entity4789 @entity1 @entity6331 @entity404 @entity310 @entity16 @entity1198 @entity4195 @entity281 @entity20383 @entity379 @entity2277 @entity2401 @entity3646 @entity340 @entity792
@entity4789 ( @entity4789 ) is an @entity792 caused by the Gram-positive bacteria @entity4195 following an untreated @entity281 in susceptible @entity1 . @entity6331 ( @entity6331 ), the most serious complication, occurs in 30-45% of @entity4789 @entity1 and leads to chronic @entity340 . Here, we focus on the genes that confer susceptibility for developing this disease. Molecular mimicry mediates the cross-reactions between streptococcal antigens and @entity1 proteins. Several autoantigens have been identified, including cardiac @entity20383 , @entity2277 , and other intracellular proteins. In heart tissue, antigen-driven oligoclonal T cell expansions probably cause the @entity6331 . These cells are @entity404 + and produce inflammatory cytokines ( @entity310 and @entity379 ). @entity3646 + cells are found in the myocardium; however, these cells are very scarce in the @entity340 of @entity6331 @entity1 . @entity3646 is a Th2-type cytokine and plays a regulatory role in the inflammatory response mediated by @entity1198 cytokines. Our findings indicate that the @entity1198 /Th2 cytokine balance has a role in healing @entity2401 while the low numbers of @entity3646 -producing cells in the valves probably induced the progressive and permanent @entity16 .
