Abstract
Rheumatic heart disease lesions are mediated by inflammatory and autoimmune reactions. Several genes related to both innate and adaptive immune responses are involved in the development of the disease. Adhesion molecules and chemokines facilitate heart tissue-T cell infiltration. T lymphocytes are the major effectors of crossreactivity between streptococcal and human proteins leading to RHD. The in vitro analysis of heart-tissue infiltrating T cells showed their ability to recognize streptococcal-M protein peptides as well as self-antigens by molecular mimicry mechanism. A cytokine balance favoring Th1 polarization and production of inflammatory cytokines and few IL-4 producing cells in the valves lead to the progression and maintenance of valvular lesions.
Highlights
IntroductionRheumatic Heart Disease (RHD) is the most serious complication of Rheumatic Fever (RF) and depends on several host factors that mediate an inflammatory and heart-tissue driven autoimmune response triggered by a protective immune response against S. pyogenes
Rheumatic Heart Disease (RHD) is the most serious complication of Rheumatic Fever (RF) and depends on several host factors that mediate an inflammatory and heart-tissue driven autoimmune response triggered by a protective immune response against S. pyogenes.RF and RHD are the most convincing examples of molecular mimicry in human pathological autoimmunity, in light of the cross reactions between streptococcal antigens and human tissue proteins, mainly heart tissue proteins, that follow throat infection by S. pyogenes in susceptible individuals.Molecular mimicry is the term used for more than 50 years [1] to define the mechanism by which self-antigens are recognized after an infection by cross reactivity
We identified oligoclonal T cell populations in the heart-tissue of RHD patients by the analysis of their T cell Receptors (TCR) that takes into consideration the molecular structure of the TCR; this T cell receptor is composed by both alpha and beta chains, which are produced through the assembly of variable (V), joining (J), and constant gene segments
Summary
Rheumatic Heart Disease (RHD) is the most serious complication of Rheumatic Fever (RF) and depends on several host factors that mediate an inflammatory and heart-tissue driven autoimmune response triggered by a protective immune response against S. pyogenes. The association of DR7 with some DQ-B or DQ-A alleles may be connected to the development of multiple valvular lesions in RHD patients in Egypt and Latvia [6,7] Beside these genes, molecular biology tools, bringing new insights about the mechanisms leading to the disease, described other genes more than 20 years later. Other genes that code for cytokines that play a role in the inflammatory reactions leading to RHD heart-tissue lesions will be briefly described. Adaptive Immune response: Rheumatic fever is characterized by inflammatory reactions and exudative modifications in joints, heart, kidney and subcutaneous tissues and nerves, being the heart lesions the most severe, leading to permanent disability. Inflammatory process: Integrins, adhesion molecules and chemokines the progression of rheumatic heart lesions
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