Prospective new biological therapies for rheumatoid arthritis

Šenolt, Ladislav; Vencovský, Jiří; Pavelka, Karel; Ospelt, Caroline

doi:10.1016/j.autrev.2009.03.010

Cited by 120 publications

(90 citation statements)

References 34 publications

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“…The interest in B cells in RA has been renewed with the introduction of powerful new therapeutic tools targeting B cells and related mediators (3)(4)(5). Characterization of the specific B cell responses will allow the identification of patients in the preclinical phase of disease as well as an understanding of the mechanism that leads to the establishment of chronic disease (7,8).…”

Section: Discussionmentioning

confidence: 99%

“…Collagenspecific B and T cell responses have been extensively studied in human RA, and B cells producing anti-CII are present in RA synovium and synovial fluid (15,17,42,43). B cells are critically important in human disease, as shown by the different therapeutic strategies in which targeting B cells ameliorate the disease (3)(4)(5). The role of B cells in RA could be essential in either the induction or the late phase of the disease during the establishment of chronic arthritis.…”

Section: Discussionmentioning

confidence: 99%

“…Several lines of evidence support an important role for B cells in the pathogenesis of RA (2)(3)(4)(5)(6). Autoantibodies, such as rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP), can precede the appearance of clinical symptoms by 10 years (7,8), suggesting that the presence of these autoantibodies can predict or interfere with the development of disease.…”

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confidence: 99%

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Characterization of the anticollagen antibody response in a new model of chronic polyarthritis

Conigliaro¹,

Benson²,

Patakas³

et al. 2011

Arthritis & Rheumatism

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Objective. Type II collagen (CII)-specific B cell responses have been recognized in human rheumatoid arthritis (RA) and in collagen-induced arthritis (CIA). An important limitation of the CIA model is that the CII response and the disease are stimulated by exogenously injected collagen. A model of experimental ovalbumin (OVA)-mediated acute arthritis has been established in which autoimmunity is spontaneous and elicited by antigen-specific T cells. This study was undertaken to create a new model of chronic autoimmune polyarthritis and characterize the associated CII-specific B cell response.Methods. Secondary challenge with OVA or CII in adjuvant was used to elicit chronic disease. CII-specific B cell responses against the epitopes U1, J1, C1, and citrullinated C1, together with the antibody affinity, were investigated in OVA-mediated arthritis.Results. Chronic autoimmune polyarthritis was induced and was dependent on the antigen used in the secondary challenge. U1 was the major CII epitope recognized, and antibodies showed the same affinity as those in CIA.Conclusion. Our findings indicate that the development and severity of chronic disease is dependent on the antigen and is associated with an increased autoreactive B cell response directed against a specific CII epitope (U1). OVA-mediated chronic arthritis exhibits anti-CII antibodies (against U1), resembling human RA and murine CIA.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Characterization of the anticollagen antibody response in a new model of chronic polyarthritis

Conigliaro¹,

Benson²,

Patakas³

et al. 2011

Arthritis & Rheumatism

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“…Gross images reprinted from (Bolon et al 2011), while the cytokine signatures were reported in (Stolina et al 2008(Stolina et al , 2009 patients with comparable conditions. Human patients with RA have similar clinical and pathological presentations, but the AIDx is nonetheless a heterogeneous condition in which some patients respond only to interleukin (IL)-1 inhibition, others improve with tumor necrosis factor-a (TNF-a) blockade, still others recover following anti-IL-6 therapy, and some are not helped by quenching any of these ''master'' cytokines (Fitzgerald et al 2005;Senolt et al 2009;Patel and Moreland 2010;Turkstra, Ng, and Schuffham 2011). Clinically equivalent demyelinating AIDx have also been shown to have divergent profiles of T-cell-derived cytokines (Segal 2010).…”

mentioning

confidence: 99%

Cellular and Molecular Mechanisms of Autoimmune Disease

Bolon

2011

Toxicol Pathol

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Autoimmune disease (AIDx) results from failure to sustain tolerance to self molecules. Dozens of AIDx involving one or multiple organ systems afflict 3% or more of people worldwide (>75% women). Predisposing factors for AIDx include genetic background, hormonal status, pathogens, and xenobiotic exposures. The incidence of AIDx is higher in individuals living in developed nations, including recent immigrants. Patients may have several AIDx simultaneously. Certain AIDx can prevent other AIDx. A history of AIDx raises the risk for developing hematopoietic neoplasia. Some common mechanisms for losing self-tolerance include reduced deletion or enhanced activation of autoreactive CD4 þ T-helper (Th) lymphocytes, defective immunomodulation by CD4 þ regulatory (Treg) and CD8 þ suppressor (Ts) T-lymphocytes, dysregulated signaling (leading to a relative increase in pro-inflammatory cytokines), comparable structure between self-antigens and foreign molecules, or expression of new epitopes on previously hidden or xenobiotic-modified self proteins. Organ-specific AIDx is generally a cell-mediated (Th1 or Th17) process, while multi-organ AIDx also incorporates a robust autoantibody (Th2) component. Cytokine signatures of different AIDx overlap incompletely; for a given AIDx, different patients have divergent cytokine profiles. Newer anti-AIDx agents are based on our increasing knowledge of AIDx pathogenesis and usually attempt to reverse lymphocyte dysfunction, quell pro-inflammatory signaling, or restore self-tolerance.

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“…Inspite the effectiveness of biologics, major side effects occur [31] exposing patients to serious infections as tuberculosis [32]. The introduction of nanotechnology in many rheumatic diseases may help refine the management armamentarium by providing the least effective dose of biologics with minimum adverse effects.…”

mentioning

confidence: 99%

Nanomedicine in rheumatology: A new field in the diagnosis and therapy of rheumatic diseases

Kenawy¹

2018

ISSN 1758-4272 Int. J. Clin. Rheumatol

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Prospective new biological therapies for rheumatoid arthritis

Cited by 120 publications

References 34 publications

Characterization of the anticollagen antibody response in a new model of chronic polyarthritis

Characterization of the anticollagen antibody response in a new model of chronic polyarthritis

Cellular and Molecular Mechanisms of Autoimmune Disease

Nanomedicine in rheumatology: A new field in the diagnosis and therapy of rheumatic diseases

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