Incidence of Rheumatic Fever in Relation to Immunologic Reactivity

Rejholec, V.; Malý, V.; Repič-Šlechta, M.; Haller, E de

doi:10.1136/ard.16.1.23

Cited by 16 publications

(5 citation statements)

References 7 publications

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“…These include genetic determinants, for example, HLAs, and the presence of certain markers such as the B-cell alloantigens (reviewed in reference 2). One of the factors originally considered in rheumatic fever susceptibility is an innate state of immune hyperresponsiveness, particularly to streptococcal antigens (12,14,16,17). While the high frequency of streptococcal infection in a population such as the one in Grenada may promote the expression of acute rheumatic fever, an alternate explanation to consider is that individuals in such an area develop or possess an innate immune hyperresponsiveness to streptococcal antigens.…”

Section: Discussionmentioning

confidence: 99%

Group A Streptococcal Antibodies in Subjects with or without Rheumatic Fever in Areas with High or Low Incidences of Rheumatic Fever

Ayoub

Nelson

Shulman

et al. 2003

Clin Vaccine Immunol

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The levels of streptococcal antibody titers in populations with or without rheumatic fever from an area with a relatively high incidence of rheumatic fever and an area with a low incidence of this disease were compared. Streptococcal antibody titers were determined for two populations, each of which included children without rheumatic fever (nonrheumatic children) and rheumatic fever patients. The two populations were derived from two separate geographic areas, one with a high incidence of rheumatic fever (Grenada) and another with a low incidence of this disease (central Florida). The results revealed an absence of consistent differences in the geometric mean antibody titers between the nonrheumatic subjects and the rheumatic fever patients from Grenada. In the population from Grenada, the mean anti-streptolysin O and anti-DNase B titers were higher in the nonrheumatic controls (P of 0.085 and 0.029, respectively). However, the mean titer of the antibody to the group A streptococcal cell wall carbohydrate was higher in the rheumatic fever patients than in the nonrheumatic controls (P ‫؍‬ 0.047). This finding contrasted with the finding that the means of all three streptococcal antibody titers in the patients with rheumatic fever were significantly higher than those in the nonrheumatic subjects from Florida (P ‫؍‬ 0.01-<0.001). The reason for this paradoxical finding became evident when the streptococcal antibody titers of the nonrheumatic subjects from Grenada and Florida were compared, revealing significantly higher levels of all three antibodies in the nonrheumatic subjects from Grenada than in the nonrheumatic subjects from Florida (P < 0.001). These results suggest that nonrheumatic individuals in an area with a high incidence of rheumatic fever have inordinately elevated levels of streptococcal antibodies in serum. The presence of elevated streptococcal antibody titers in such a population, which probably reflects a high background prevalence of streptococcal infections, should be taken into consideration when evaluating the role of the group A streptococcus in nonpurulent complications of infections.

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Section: Discussionmentioning

confidence: 99%

Group A Streptococcal Antibodies in Subjects with or without Rheumatic Fever in Areas with High or Low Incidences of Rheumatic Fever

Ayoub

Nelson

Shulman

et al. 2003

Clin Vaccine Immunol

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“…These mitogens were also found to sustain human immunodeficiency virus type 1 replication after stimulation of T cells with the virus (3). Because of the numerous immunomodulating activities of SM and its fractions, it is possible to envisage an important role for such molecules in determining the outcomes of infections with group A streptococci and a relevance to the pathogenesis of rheumatic fever (RF), the mechanism of which is still poorly understood (5,37,39,42).…”

mentioning

confidence: 99%

Antibody levels and in vitro lymphoproliferative responses to Streptococcus pyogenes erythrogenic toxin A and mitogen of patients with rheumatic fever

et al. 1991

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We investigated the in vitro lymphoproliferative responses to a streptococcal mitogen and erythrogenic toxin A of children with acute rheumatic fever (ARF) and patients with chronic rheumatic heart disease (CRHD). Antibody levels to the streptococcal products were also analyzed in the sera of those with ARF or chronic rheumatic heart disease as well as in the sera of children with streptococcal pharyngitis or poststreptococcal glomerulonephritis. Our results demonstrated that the individuals had depressed lymphoproliferative responses during the active stage of rheumatic fever. The depressed responses were not found either to be induced by time-sensitive mitogen-specific suppressor cells or to be related to a dose-response phenomenon. On the other hand, antibody levels to the extracellular mitogens were significantly elevated in the sera of children with ARF compared with the levels in the rest of the groups. The hyperresponsiveness noted among children with ARF was found to be at a quantitative level and was not due to recognition of more epitopes, as determined by Western blotting (immunoblotting). The proffle of immune responsiveness in children with ARF to the streptococcal extracellular mitogens is discussed in relation to the pathogenesis of disease.

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“…Early but unconfirmed studies suggested that susceptibility to rheumatic fever followed a simple autosomal recessive pattern of inheritance (4)(5)(6), or paralleled the inheritance of ABO blood group or ABO secretor status (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17). The pathogenesis of rheumatic fever is also thought to involve an aberrant immunological reaction, either humoral or cellular, or both, triggered by an antecedant group A streptococcal infection (18)(19)(20)(21)(22)(23)(24)(25). Since cell surface antigens encoded by the genes of the major histocompatibility complex are known to be important in controlling immunological responsiveness, recent genetic studies have examined the association between rheumatic fever and HLA antigens.…”

Section: Introductionmentioning

confidence: 99%

Association of class II human histocompatibility leukocyte antigens with rheumatic fever.

Ayoub¹,

Barrett²,

Maclaren³

et al. 1986

J. Clin. Invest.

170

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The association of class I and II HLA antigens with rheumatic fever and its manifestations was examined in 72 patients, including 48 blacks and 24 Caucasians. No significant association was found between class I antigens and rheumatic fever. In contrast, HLA-DR2 and HLA-DR4 phenotypes were encountered in a significantly higher frequency in black and Caucasian patients with rheumatic fever, respectively, compared with the control populations (P < 0.005). The most significant association (P < 0.005) of these DR antigens with a major manifestation of rheumatic fever was found for mitral insufficiency. In addition, a significant association was encountered between persistent elevation of antibody to the group A streptococcal carbohydrate and HLA-DR4 in Caucasian patients (P < 0.04) or HLA-DR2 in the black patients (P < 0.001). The frequency of HLA-DR2/ 4 heterozygotes among patients with rheumatic fever did not differ significantly from controls. These findings support the concept of a genetically determined susceptibility to rheumatic fever and, particularly, to rheumatic heart disease. The association of the clinical manifestations of rheumatic fever and the immune hyperresponsiveness to a streptococcal antigen could be ascribed to a disease-associated immune-response gene which is in linkage disequilibrium with the DR2 and DR4 alleles of HLA-DR locus on chromosome six.

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Incidence of Rheumatic Fever in Relation to Immunologic Reactivity

Cited by 16 publications

References 7 publications

Group A Streptococcal Antibodies in Subjects with or without Rheumatic Fever in Areas with High or Low Incidences of Rheumatic Fever

Group A Streptococcal Antibodies in Subjects with or without Rheumatic Fever in Areas with High or Low Incidences of Rheumatic Fever

Antibody levels and in vitro lymphoproliferative responses to Streptococcus pyogenes erythrogenic toxin A and mitogen of patients with rheumatic fever

Association of class II human histocompatibility leukocyte antigens with rheumatic fever.

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