Reduced anti-TNFα autoantibody levels coincide with flare in systemic lupus erythematosus

Sjöwall, Christopher; Ernerudh, Jan; Bengtsson, Anders; Sturfelt, Gunnar; Skogh, Thomas

doi:10.1016/j.jaut.2004.02.003

Cited by 41 publications

(26 citation statements)

References 41 publications

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“…It is suggested that the failure of TGFβ1-dependent down-regulation of IgG production in SLE might lead to hyperactive plasma cells, and the IgG production correlates well with the amount of IgG -TGFβ1 complexes. Increased amounts of these were found both in the sera of active and inactive SLE patients without statistically significant difference between the two groups [30]. These complexes may have deleterious effects on host defence against microbial infections.…”

Section: Discussionmentioning

confidence: 88%

Expression of TGFβ1 and Its Signaling Components by Peripheral Lymphocytes in Systemic Lupus Erythematosus

Kohut

Hajdú

Gergely

et al. 2008

Pathol. Oncol. Res.

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Transforming growth factor beta1 (TGFbeta1) is an important immunosuppressive cytokine. Defects in its production by lymphocytes and the failure of TGFbeta1 to regulate immunological functions have been described in SLE. Expression of TGFbeta1 and the related signaling pathway was studied in the peripheral lymphocytes of SLE patients. The total plasma TGFbeta1 level in active and inactive SLE patients compared to healthy controls was also measured. TGFbeta1 and all downstream signaling elements were expressed in normal cells. However, in more than 50% of SLE patients the isolated T cell population showed no TGFbeta1 mRNA expression and at least one member of the TGFbeta1 pathway was also missing (TGFbeta-RI, Smad2 and Smad3) in more than half of the patients. Total plasma TGFbeta1 level was increased in both active and inactive SLE groups compared to normal controls (p< 0.05). These data raise questions about the availability of TGFbeta1 signaling in lymphocytes in SLE patients, however, the elevated total plasma TGFbeta1 level suggests that the failure of TGFbeta1 effects is not the consequence of low level of this cytokine in SLE.

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Section: Discussionmentioning

confidence: 88%

Expression of TGFβ1 and Its Signaling Components by Peripheral Lymphocytes in Systemic Lupus Erythematosus

Kohut

Hajdú

Gergely

et al. 2008

Pathol. Oncol. Res.

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“…AAbs directed against TNFα were identified in SLE patients [59] and according to the putative inflammatory role of TNFα in SLE organ disease, anti-TNFα AAb serum levels were inversely correlated with the severity of the disease and directly correlated with serum concentrations of complement factors C1q and C3. Interestingly, although TNFα-blocking therapies frequently induce anti-nuclear and antinative DNA AAbs in the serum of treated patients, they are fortunately rarely associated with clinical lupus-like syndromes [60][61][62][63].…”

Section: Anti-tnfα Autoantibodiesmentioning

confidence: 99%

“…The physiological significance of these natural antibodies remains poorly understood. It has been proposed that natural neutralizing anti-cytokine AAbs could scavenge pro-inflammatory cytokines and thereby limit the diffusion of these cytokines beyond active sites of inflammation, thus preventing systemic deleterious effects and distal tissue damage [59,107]. Alternatively, some natural anti-cytokine AAbs may behave as carrier proteins, providing a reservoir of cytokines, thus increasing their half-life and modulating their bioactivity as previously shown with exogenous cytokines [112,113].…”

Section: Anti-cytokine Autoantibodies In Healthy Subjectsmentioning

confidence: 99%

Emerging clinical phenotypes associated with anti-cytokine autoantibodies

Vincent

Plawecki

Goulabchand

et al. 2015

Autoimmunity Reviews

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“…However, although raised circulating levels of many pro-inflammatory cytokines are seen, in some instances paralleling disease activity [73], cytokine levels (including IL-6) have not been found to correlate with circulating CRP in SLE [73,74]. Neither does the presence of autoantibodies to CRP-regulating cytokines offer an explanation to the modest CRP response in SLE [75]. Genetic polymorphisms of CRP-inducing cytokines and their concomitant receptors have, however, been found to be associated with SLE and might predispose to distinct clinical and immunological features [76][77][78].…”

Section: Crp In Sle Crp In Atherosclerosismentioning

confidence: 99%

CRP and Anti-CRP Autoantibodies in Systemic Lupus Erythematosus

Sjöwall¹,

Bengtsson²

2005

CRR

Self Cite

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Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by multiple organ involvement, production of a wide range of autoantibodies and by formation and tissue deposition of immune complexes in the inflamed organs. In contrast to most systemic inflammatory conditions, and despite raised levels of pro-inflammatory cytokines, SLE flares are rarely reflected by elevated C-reactive protein (CRP), an important acute-phase reactant in man with homologues in vertebrates and several invertebrates. Normally, the circulating concentration of liver-derived CRP rises rapidly in response to infections and tissue injury, and CRP measurement is widely employed as a marker of ongoing inflammation. With sensitive methods, detection of small elevations of CRP is also valuable as a prognostic marker in cardiovascular disease. As a part of the innate immune system, CRP binds certain molecules exposed on the surface of dying cells/apoptotic bodies and on the surface of pathogens and mediates their elimination by uptake in the reticuloendothelial system. CRP also interacts with IgG-containing immune complexes, binds Fc-receptors and activates the complement system via C1q. In murine lupus, CRP has been found to decrease autoantibody levels and increase the survival rates. In this review we discuss possible explanations for, and consequences of, the relative CRP failure in SLE, as well as pathogenetic implications of anti-CRP autoantibodies.

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Reduced anti-TNFα autoantibody levels coincide with flare in systemic lupus erythematosus

Cited by 41 publications

References 41 publications

Expression of TGFβ1 and Its Signaling Components by Peripheral Lymphocytes in Systemic Lupus Erythematosus

Expression of TGFβ1 and Its Signaling Components by Peripheral Lymphocytes in Systemic Lupus Erythematosus

Emerging clinical phenotypes associated with anti-cytokine autoantibodies

CRP and Anti-CRP Autoantibodies in Systemic Lupus Erythematosus

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