Frequencies of epstein‐barr virus—inducible IgM anti‐IgG B lymphocytes in normal children and children with juvenile rheumatoid arthritis

Fong, Sherman; Miller, John J.; Moore, Terry L.; Tsoukas, Constantine D.; Vaughan, John H.; Carson, Dennis A.

doi:10.1002/art.1780250808

Cited by 22 publications

(4 citation statements)

References 22 publications

(12 reference statements)

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“…However, the EBV has not been as extensively examined in relation to JIA. The outcomes of three small studies seeking evidence of an increased frequency of the EBV infection in JIA have been conflicting [47][48][49]. In 2002, Massa et al [28] examined the interaction between the HLA type and EBV infection in oligoarticular JIA.…”

Section: Infectionmentioning

confidence: 99%

Possible environmental determinants of juvenile idiopathic arthritis

Ellis¹,

Munro²,

Ponsonby³

2009

Rheumatology

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Like other autoimmune diseases, including adult RA, risk of developing juvenile idiopathic arthritis (JIA) is thought to be determined by a complex combination of genetic and environmental factors. Although some predisposing JIA genes are now being identified, research aimed at identifying environmental influences lags behind most other autoimmune conditions. Here we review research to date, from which some evidence has been generated to support a role for breastfeeding, infection and maternal smoking in determining JIA risk. We also propose further hypotheses worthy of testing, based on knowledge acquired for other autoimmune diseases. These include the role of vitamin D and sun exposure, and the role of early-life infection ('the hygiene hypothesis') in determining risk. Finally, we discuss future directions including practical study designs to more comprehensively test hypotheses and provide new insight into this important area of research.

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Section: Infectionmentioning

confidence: 99%

Possible environmental determinants of juvenile idiopathic arthritis

Ellis¹,

Munro²,

Ponsonby³

2009

Rheumatology

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“…These data suggested that by young adult hood the expansion of IgM RF autoantibody precursor cells had occurred, only to be ex pressed after stimulation with an exogenous B cell activator. This was confirmed by a direct analysis of the number of IgM RF-producing B cells in children [16]. Normal, healthy children had EBV-inducible RF pre cursor B cell frequencies lower than adults, but higher than neonates ( fig.…”

Section: Age-associated Expression O F Two Human Autoantibodiesmentioning

confidence: 48%

Origin and Age-Associated Changes in the Expression of a Physiologic Autoantibody

Fong¹,

Chen²,

Vaughan³

et al. 1985

Gerontology

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Aging is accompanied by increased prevalence of serum autoantibodies. One commonly detected autoantibody, IgM rheumatoid factor, is also found associated with rheumatoid arthritis and other autoimmune disorders. Much evidence indicates that this autoantibody plays a physiologic role in the immune response. The potential of human subjects to secrete this autoantibody and the age-related changes in its expression by human peripheral blood and bone marrow lymphocytes have been investigated. The size of this self-reactive B cell pool increases with advancing age. The lymphocytes expressing this potential are found predominantly in an early B cell subset in elderly individuals as compared to a more mature B cell subset in individuals with rheumatoid arthritis. Preliminary data show that IgM rheumatoid factors share idiotypes implying a common origin, possible from a single light chain gene or a closely related family of light chain genes.

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“…The mechanism of onset of SS is unknown, but some reports have suggested the participation of Epstein-Barr virus (EBV). For example, EBVcauses polyclonal activation of B cells (2)(3)(4), EBV can establish B cell lines positive for EBVassociated nuclear antigen (EBNA), which is expressed spontaneously (that is, without stimulation) by peripheral lymphocytes in SS (3), histopathological changes in SS resemble those in epipharyngeal carcinoma (5), and anti-SS-B antibody forms deposits with cytoplasmic proteins containing EBV-encoded RNA (6). We encountered a patient with rheumatoid arthritis (RA) who developed SS after repeated infectious mononucleosislike symptomsduring the course of RA, and in whom reactivation of EBVwas suspected to have participated in the onset of SS.…”

Section: Introductionmentioning

confidence: 99%