Serial studies on the cellular immune response to streptococcal antigens in acute and convalescent rheumatic fever patients in Trinidad

Read, Stanley; Reid, H. F. M.; Fischetti, Vincent A.; Poon-King, Theo; Ramkissoon, R.; McDowell, Mary Ann; Zabriskie, John B.

doi:10.1007/bf00915249

Cited by 47 publications

(18 citation statements)

References 13 publications

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“…Historically, previous studies have indicated that lymphocytes were highly responsive to streptococcal cell wall and membrane antigens (450)(451)(452). T-cell responses to M proteins have been investi-gated in a number of studies (138,216,435,436,455,456,(521)(522)(523).…”

Section: Autoimmunity and Molecular Mimicry In Rheumatic Fevermentioning

confidence: 99%

Pathogenesis of Group A Streptococcal Infections

Cunningham

2000

Clinical Microbiology Reviews

1,607

1,337

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Section: Autoimmunity and Molecular Mimicry In Rheumatic Fevermentioning

confidence: 99%

Pathogenesis of Group A Streptococcal Infections

Cunningham

2000

Clinical Microbiology Reviews

1,607

1,337

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“…Acute RF (ARF) patients' lymphocytes have exacerbated in vitro cellular reactivity as compared to patients with acute post-streptococcal glomerulonephritis peaking at 1-6 months and lasting for at least 2 years after onset [45]. Upon stimulation, acute ARF patients' peripheral blood mononuclear cells (PBMC) produce larger amounts of IL-1 and IL-2 than PBMC from normal controls, streptococcal pharyngitis (SP), or chronic rheumatic heart disease (CRHD) patients, and the IL-2 overproduction persisted after 48 weeks.…”

Section: Cytokines In Rheumatic Fevermentioning

confidence: 99%

Understanding rheumatic fever

2011

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Through a comprehensive review of the recent findings on rheumatic fever, we intend to propose a new physiopathologic model for this disease. A Medline search was performed for all articles containing the terms rheumatic fever or rheumatic heart disease in title or abstract from 1970 to 2011. Best evidence qualitative technique was used to select the most relevant. The scientific interest on rheumatic fever has notably diminished throughout the twentieth century as evidenced by the comparison of the proportion of articles in which RF was a subject in 1950 (0.26%) and today (0.03%) [Pubmed]. However, RF remains a major medical and social problem in the developing world and in the so-called hotspots, where it still causes around 500.000 deaths each year, not too different from the pre-antibiotic era. The role of genetic factors in RF susceptibility is discussed. Familiar aggregation, similarity of disease patterns between siblings, identical twin, and HLA correlation studies are evidence for a genetic influence on RF susceptibility. The suspect-involved genes fall mainly into those capable of immunologic mediation. Molecular mimicry explains the triggering of RF, but an intense and sustained inflammation is needed to cause sequels. Also, RF patients vary greatly in terms of symptoms. It is likely that a genetic background directing immune response towards a predominantly Th1 or Th2 pattern contributes to these features. The recent findings on rheumatic fever provide important insight on its physiopathology that helps understanding this prototype post-infectious autoimmune disease giving insights on other autoimmune conditions.

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“…The delay in manifestations of ARF following infection and the presence of infiltrates of Tehelper lymphocytes and macrophages in acute rheumatic valvulitis and B cells in Aschoff body suggests an important role of the immune system in the pathogenesis of this disease [6,7]. There has been a controversy over the phenotypic characteristics of T lymphocytes in the peripheral blood of ARF/RHD patients.…”

Section: Introductionmentioning

confidence: 99%