Tumor necrosis factor‐α messenger RNA expression in patients with relapsing‐remitting multiple sclerosis is associated with disease activity

Rieckmann, Peter; Albrecht, M.; Kitze, Bernd; Weber, Thomas K.; Tumani, Hayrettin; Broocks, Andreas; Lüer, W.; Helwig, A; Poser, S.

doi:10.1002/ana.410370115

Cited by 326 publications

(154 citation statements)

References 34 publications

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“…Odds ratios showed a statistically significant association between antigen-specific T cell response to MOBP and exacerbations of MS. Thus, our study extends previous work demonstrating a correlation of changes in immune responses with increased MRI activity (Calabresi et al, 1998a;Oger et al, 1988;Prat et al, 2000;Rieckmann et al, 1995). Due to sample size available, our initial studies were limited to analyses to MOBP aa 1-19, MOBP aa 11-29, MOBP aa 20-38, MOBP aa 31-49, MOBP aa 41-59 and bovine MBP.…”

Section: Discussionsupporting

confidence: 79%

A new approach for evaluating antigen-specific T cell responses to myelin antigens during the course of multiple sclerosis

Arbour

Holz

Sipe

et al. 2003

Journal of Neuroimmunology

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We used a flow cytometry assay to measure proliferation and cytokine production of self-antigenspecific T cells in individual patients during the clinical course of multiple sclerosis (MS). Myelinassociated oligodendrocytic basic protein (MOBP) was selected for proof of principles in the assay, along with myelin basic protein (MBP) to assess specific activated T cells in 10 MS patients over an 18-month period, in parallel with brain magnetic resonance imaging (MRI) scans and clinical rating scale. A positive correlation occurred between antigen-specific T cell proliferation and interferon-γ production with clinical relapses and MRI lesion activity that was absent when the same patients were in remission.

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Section: Discussionsupporting

confidence: 79%

A new approach for evaluating antigen-specific T cell responses to myelin antigens during the course of multiple sclerosis

Arbour

Holz

Sipe

et al. 2003

Journal of Neuroimmunology

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Section: Discussionmentioning

confidence: 99%

“…Increased IFN-~ and TNF-ot activity (30) and increased TNF-ct and TNF-[3 m R N A levels (31) occur in PBL of MS patients before both clinical relapse and active magnetic resonance scans (31). Relapse in MS has also been associated with decreased expression o f the antiinflammatory cytokines TGF-[3 and IL-10 in MS (31). Similarly, inflammatory cytokines have been demonstrated in the CNS during active EAE (32)(33)(34), whereas recovery has been associated with concomitant decreased CNS expression of IFN-% IL-2, IL-4, and IL-6 and increased expression of IL-10 m R N A (35).…”

Section: Discussionmentioning

confidence: 99%

A predictable sequential determinant spreading cascade invariably accompanies progression of experimental autoimmune encephalomyelitis: a basis for peptide-specific therapy after onset of clinical disease.

Johnson

Tuohy

1996

The Journal of Experimental Medicine

256

185

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SummaryThe development of autoimmune disease is accompanied by the acquired recognition of new self-determinants, a process commonly referred to as determinant spreading. In this study, we addressed the question of whether determinant spreading is pathogenic for progression of chronic-relapsing experimental autoimmune encephalomyelitis (EAE), a disease with many similarities to multiple sclerosis (MS). Our approach involved a systematic epitope mapping of responses to myelin proteolipid protein (PLP) as well as assaying responses to known encephalitogenic determinants of myelin basic protein (MBP 87-99) and myelin oligodendrocyte g|yco-protein (MOG 92-106) at various times after induction of EAE in (SWRXSJL)F1 mice immunized with PLP 139-151. We found that the order in which new determinants are recognized during the course of disease follows a predictable sequential pattem. At monthly intervals after immunization with p139-151, responses to PLP 249-273, MBP 87-99, and PLP 173-198 were sequentially accumulated in all mice examined. Three lines of evidence showed that determinant spreading is pathogenic for disease progression: (a) spreading determinants mediate passive transfer of acute EAE in naive (S'W~• 1 recipients; (b) an invariant relationship exists between the development of relapse/progression and the spreading of recognition to new immunodominant encephalitogenic determinants; and (c) after EAE onset, the induction ofpeptidespecific tolerance to spreading but not to nonspreading encephalitogenic determinants prevents subsequent progression of EAE. Thus, the predictability of acquired self-determinant recognition provides a basis for sequential determinant-specific therapeutic intervention after onset of the autoimmune disease process.

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“…In addition, transgenic mice that constitutively expressed a trans-dominant form of IB␣ displayed lower incidence and severity of collagen-induced arthritis, an animal model of human rheumatoid arthritis (47). AP-1 and/or NF-B induce the expression of cytokines and chemokines involved in EAE and MS. Tumor necrosis factor ␣ (TNF␣) has been shown to activate both AP-1 and NF-B, and TNF␣ is a potent pro-inflammatory cytokine that plays an important role in MS (48,49). Matrix metalloproteinase-9 (MMP-9), which is regulated by AP-1 and NF-B, also plays a crucial role in lymphocyte recruitment to the central nervous system in MS, and patients with MS show high levels of MMP-9 in the cerebrospinal fluid (50,51).…”

Section: Discussionmentioning

confidence: 99%

The SWI/SNF Chromatin-remodeling Complex Modulates Peripheral T Cell Activation and Proliferation by Controlling AP-1 Expression

Jeong

Lee²,

Lee³

et al. 2010

Journal of Biological Chemistry

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The SWI/SNF chromatin-remodeling complex has been implicated in the activation and proliferation of T cells. After T cell receptor signaling, the SWI/SNF complex rapidly associates with chromatin and controls gene expression in T cells. However, the process by which the SWI/SNF complex regulates peripheral T cell activation has not been elucidated. In this study, we show that the SWI/SNF complex regulates cytokine production and proliferation of T cells. During T cell activation, the SWI/SNF complex is recruited to the promoter of the transcription factor AP-1, and it increases the expression of AP-1. Increased expression of the SWI/SNF complex resulted in enhanced AP-1 activity, cytokine production, and proliferation of peripheral T cells, whereas knockdown of the SWI/SNF complex expression impaired the AP-1 expression and reduced the activation and proliferation of T cells. Moreover, mice that constitutively expressed the SWI/SNF complex in T cells were much more susceptible to experimentally induced autoimmune encephalomyelitis than the normal mice were. These results suggest that the SWI/SNF complex plays a critical role during T cell activation and subsequent immune responses.

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Tumor necrosis factor‐α messenger RNA expression in patients with relapsing‐remitting multiple sclerosis is associated with disease activity

Cited by 326 publications

References 34 publications

A new approach for evaluating antigen-specific T cell responses to myelin antigens during the course of multiple sclerosis

A new approach for evaluating antigen-specific T cell responses to myelin antigens during the course of multiple sclerosis

A predictable sequential determinant spreading cascade invariably accompanies progression of experimental autoimmune encephalomyelitis: a basis for peptide-specific therapy after onset of clinical disease.

The SWI/SNF Chromatin-remodeling Complex Modulates Peripheral T Cell Activation and Proliferation by Controlling AP-1 Expression

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