Lymphocytes binding C-reactive protein during acute rheumatic fever.

Williams, Ralph C.; Kilpatrick, Kathleen A.; Kassaby, Mahitab El; Abdin, Z H

doi:10.1172/jci109056

Cited by 26 publications

(9 citation statements)

References 46 publications

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“…Human CRP is known to bind to Ag-induced T cells (44) and also to B cells (45), and it was recently established that human CRP binds with high affinity to the activation receptor Fc␥RI and the inhibitory receptor Fc␥RIIb in both mice and humans (8 -11). Notably, there is growing evidence that Fc␥RIIb plays a major inhibitory role in controlling the emergence of autoimmune disease (46,47).…”

Section: Discussionmentioning

confidence: 99%

Experimental Allergic Encephalomyelitis Is Inhibited in Transgenic Mice Expressing Human C-Reactive Protein

Szalai

Nataf

et al. 2002

The Journal of Immunology

107

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We show here using a transgenic model that human C-reactive protein (CRP) protects against experimental allergic encephalomyelitis (EAE) in C57BL/6 mice. In transgenic compared with wild-type females, the duration of the human CRP acute phase response that accompanies the inductive phase of active EAE correlates with a delay in disease onset. In transgenic males, which have higher human CRP expression than females do, EAE is delayed, and its severity is reduced relative to same-sex controls. Furthermore, in male transgenics, there is little or no infiltration of the spinal cord by CD3+ T cells and CD11b+ monocytes and macrophages, and EAE is sometimes prevented altogether. CRP transgenics also resist EAE induced passively by transfer of encephalitogenic T cells from wild-type donors. Human CRP has three effects on cultured encephalitogenic cells that could contribute to the protective effect observed in vivo: 1) CRP inhibits encephalitogenic peptide-induced proliferation of T cells; 2) CRP inhibits production of inflammatory cytokines (TNF-α, IFN-γ) and chemokines (macrophage-inflammatory protein-1α, RANTES, monocyte chemoattractant protein-1); and 3) CRP increases IL-10 production. All three of these actions are realized in vitro only in the presence of high concentrations of human CRP. The combined data suggest that during the acute phase of inflammation accompanying EAE, the high level of circulating human CRP that is achieved in CRP-transgenic mice inhibits the damaging action of inflammatory cells and/or T cells that otherwise support onset and development of EAE.

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Section: Discussionmentioning

confidence: 99%

Experimental Allergic Encephalomyelitis Is Inhibited in Transgenic Mice Expressing Human C-Reactive Protein

Szalai

Nataf

et al. 2002

The Journal of Immunology

107

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show abstract

“…CRP has multiple biological actions including calcium-dependent binding to phosphocholine, fibronectin, chromatin, histones, and ribonucleoprotein, induction of the expression of adhesion molecules on endothelial cells (Pasceri et al, 2000), binding to specific receptors on leukocytes resulting in modulation of function (Mortensen and Zhong, 2000), and activation of the classical complement pathway (Volanakis, 1982) by binding to C1q (Williams et al, 1978). Unlike IgG, which specifically recognizes distinct epitopes, CRP appears to recognize altered self and foreign molecules (du Clos, 2000).…”

Section: Discussionmentioning

confidence: 99%

C-Reactive-Protein-Associated Increase in Myocardial Infarct Size After Ischemia/Reperfusion

Barrett

Hennan

Marks

et al. 2002

J Pharmacol Exp Ther

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C-Reactive protein (CRP), a marker for acute inflammation, is associated with increased risk of cardiovascular events. The mechanism underlying this association is uncertain. An acute inflammatory response was induced in rabbits by subcutaneous injection of croton oil (CO) 1 to 3 days before 30 min of regional myocardial ischemia/180 min of reperfusion. CO treatment increased plasma CRP from below the limit of detection to 2.5 Ϯ 0.5 mg/dl and was associated with an increase in infarct size expressed as percentage of risk region [32 Ϯ 6% vehicle controls (n ϭ 7) to 47 Ϯ 9% CO-treated rabbits (n ϭ 7; P Ͻ 0.05]. After 10 min of ischemia and 180 min reperfusion, no infarct was found in controls; however, an infarct of 7 Ϯ 1% was found in CO-treated rabbits (P Ͻ 0.05; CRP, 2.3 Ϯ 0.4 mg/dl). The CRP-related increase in infarct size was not observed in croton oil-treated, C6-deficient rabbits (n ϭ 5/group), indicating the involvement of complement. In these rabbits, infarct size was 22 Ϯ 2% (P Ͻ 0.05) despite having plasma CRP of 4.3 Ϯ 0.4 mg/dl. The CRP-associated increase in infarct size was ameliorated by pretreatment with heparin (n ϭ 7; infarct size 33 Ϯ 3%; CRP, 2.3 Ϯ 0.3 mg/dl; P Ͻ 0.05) or N-acetylheparin (n ϭ 7; infarct size 23 Ϯ 4%; CRP, 3.1 Ϯ 0.5 mg/dl; P Ͻ 0.05). These observations may explain why increased serum CRP is associated with an augmented risk for cardiovascular events.

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“…In some experiments, lvmphocytes were separated into erythrocyte (E)-rosetting and nonrosetting stubpopulaltions using neuraiminidase E rosettes and centrifugation through a Ficoll-triosil gradient as previously described (21). Nonrosetting cells at the Ficoll-triosil interface were almost entirely B and "null" cells as indicated by fluoreseence staining for surface immunoglobtulin uising pepsin-digested rabbit anti-human immunoglobtulin (21) as well as by' staining with chicken anti-human Ila antibody followed by goatt anti-chicken y-globuliin fluioresceinalted aintibody (22, 2:3 (15,16). 1 wk after the third injection of pooled SLE lymphocytes, rabbits were bled out and antisenim absorbed.…”

Section: Methodsmentioning

confidence: 99%

Lymphocyte antigens in systemic lupus erythematosus: studies with heterologous antisera.

Williams¹,

Hughes²,

Snaith³

et al. 1980

J. Clin. Invest.

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Lymphocytes binding C-reactive protein during acute rheumatic fever.

Abstract: A B S T R A C T Lymphocytes binding

Cited by 26 publications

References 46 publications

Experimental Allergic Encephalomyelitis Is Inhibited in Transgenic Mice Expressing Human C-Reactive Protein

Experimental Allergic Encephalomyelitis Is Inhibited in Transgenic Mice Expressing Human C-Reactive Protein

C-Reactive-Protein-Associated Increase in Myocardial Infarct Size After Ischemia/Reperfusion

Lymphocyte antigens in systemic lupus erythematosus: studies with heterologous antisera.

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