Infliximab but not etanercept induces apoptosis in lamina propria T-lymphocytes from patients with Crohn’s disease

Brande, Jan M. H. van den; Braat, Henri; Brink, Gijs R. van den; Versteeg, Henri H.; Bauer, Christiaan A; Hoedemaeker, Inge; Montfrans, Catherine van; Hommes, Daan W.; Peppelenbosch, Maikel P.; Deventer, S. J. H. Van

doi:10.1016/s0016-5085(03)00382-2

Cited by 675 publications

(408 citation statements)

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“…In a murine model of chronic TB, neutralization of TNF by antibody but not the TNFR fusion molecule exacerbated chronic TB because of better penetration of antibodies into granulomas (19). In humans, higher avidity and better stability of membrane-bound TNF was demonstrated with anti-TNF mAb (20), which in some studies leads to more efficient apoptosis (21)(22)(23).…”

Section: Discussionmentioning

confidence: 99%

Risk of tuberculosis is higher with anti–tumor necrosis factor monoclonal antibody therapy than with soluble tumor necrosis factor receptor therapy: The three‐year prospective french research axed on tolerance of biotherapies registry

Tubach

Salmon

Ravaud

et al. 2009

Arthritis & Rheumatism

576

366

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Objective. Tuberculosis (TB) is associated with anti-tumor necrosis factor (anti-TNF) monoclonal antibody (mAb) therapy, but whether this association is drug-specific remains a concern. Our objective was to describe cases of TB associated with anti-TNF mAb therapy, identify risk factors, and estimate the incidence.Methods. We conducted an incidence study and a case-control analysis to investigate the risk of newly diagnosed TB associated with the use of anti-TNF agents. As part of the French Research Axed on Tolerance of Biotherapies (RATIO) registry, for 3 years we collected cases of TB among French patients receiving anti-TNF mAb therapy for any indication; for each case, 2 patients treated with anti-TNF agents served as control subjects.Results. We collected 69 cases of TB in patients treated for rheumatoid arthritis (n ‫؍‬ 40), spondylarthritides (n ‫؍‬ 18), inflammatory colitis (n ‫؍‬ 9), psoriasis (n ‫؍‬ 1) and Behçet's disease (n ‫؍‬ 1) with infliximab (n ‫؍‬ 36), adalimumab (n ‫؍‬ 28), and etanercept (n ‫؍‬ 5). None of the patients had received correct chemoprophylactic treatment. The sex-and ageadjusted incidence rate of TB was 116.7 per 100,000 patient-years. The standardized incidence ratio (

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Section: Discussionmentioning

confidence: 99%

Risk of tuberculosis is higher with anti–tumor necrosis factor monoclonal antibody therapy than with soluble tumor necrosis factor receptor therapy: The three‐year prospective french research axed on tolerance of biotherapies registry

Tubach

Salmon

Ravaud

et al. 2009

Arthritis & Rheumatism

576

366

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“…As many patients with IBD were either refractory or intolerant to treat ment with the classic agents already discussed, there was an urgent need for the development of more specific novel therapeutic approaches. In this context, anti TNF agents, including infliximab, adalimumab, golimumab and certo lizumab pegol, were introduced into clin ical therapy for IBD 14,[23][24][25][26][27][28][29][30][31][32][33] . For instance, infliximab was shown to be effective for induction and maintenance of remission in both Crohn's disease and ulcerative colitis as well as for treatment of fistulas in Crohn's disease, highlighting the broad relevance of anti TNF therapy 14,24 .…”

Section: Classic Immunosuppressive Drugsmentioning

confidence: 99%

Current and emerging therapeutic targets for IBD

Neurath

2017

Nat Rev Gastroenterol Hepatol

512

403

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Inflammatory bowel diseases (including IBD, exempli fied by Crohn's disease and ulcerative colitis) are chronic relapsing disorders affecting the gastrointestinal tract. IBD has a progressive and destructive nature and, there fore, can cause various complications including steno ses, abscesses, fistulas, extraintestinal manifestations and colitis associated neoplasias and cancer 1,2 . Thus, effective therapeutic approaches are of high clinical rele vance in patients with IBD. This Review summarizes current therapeutic strategies and highlights emerging new treatment approaches for IBD with special refer ence to the proposed molecular mechanisms of action of anti inflammatory drugs. Current IBD therapiesClassic anti-inflammatory drugs. 5 Aminosalicylates (5 ASAs) are important anti inflammatory drugs that are frequently used for anti inflammatory therapy in patients with ulcerative colitis 3 . By contrast, 5 ASA based drugs show little or no efficacy in inducing res olution of clinical symptoms and tissue inflammation in patients with Crohn's disease 4 .5 ASAs are effective for induction and mainten ance of remission in ulcerative colitis and might also reduce the risk of developing colitis associated tumours in these patients 5 . Several mechanisms of action for 5 ASAs have been proposed, including reduction of prostaglandin synthesis via inhibition of cyclooxygenase, suppression of proinflammatory cytokine production and oxygen free radicals, inhib ition of lipoxygenase, blockade of neutrophil chemo taxis and mast cell activation, and impairment of nuclear factor κB activation (NF κB) in immune cells 3 . Moreover, studies in mice revealed that 5 ASA based drugs augment peroxisome proliferator activated receptor γ (PPARγ) expression and promote PPARγ translocation from the cytoplasm to the nucleus where they result in activation of peroxisome proliferator hormone response element driven genes to suppress colitis activity 6,7 .In addition to 5 ASAs, corticosteroids (systemically or topically delivered) have been used for remission induction in ulcerative colitis 2 . Although cortico steroids favour induction of remission in both ulcer ative colitis and Crohn's disease, they are not suitable for mainten ance of remission in IBD 1,2 . Mechanistically, gluco corticoids bind to a specific cytosolic receptor fol lowed by translocation of the complex to the nucleus to either activate or repress gene transcription (via bind ing to DNA corticosteroid response elements) 8,9 . Additionally, the glucocorticoid-receptor complex can inactivate pro inflammatory transcription factors such as NF κB and activator protein 1 (AP1) via proteinprotein inter actions, thereby preventing their activation of inflammatory mediators (for example, leukotrienes and cytokines such as IL 1 and IL 6). REVIEWS© 2 0 1 7 M a c m i l l a n P u b l i s h e r s L i m i t e d , p a r t o f S p r i n g e r N a t u r e . A l l r i g h t s r e s e r v e d .

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“…Newer data suggest that the cross-linking of anti-TNF Ab on the cell is responsible for its reverse intracellular signaling, inhibiting the production of inflammatory cytokines, inducing apoptosis, and causing growth arrest. A few studies have shown differential binding of different anti-TNF agents to soluble versus membrane TNF with ensuing differences in ability to induce apoptosis in cells, although the results have been variable [17,18].…”

Section: Intracellular Signaling Mediated By Anti-tnfα Agentsmentioning

confidence: 99%

“…One study compared the abilities of ETA and INF to neutralize TNF and to induce apoptosis in vitro [17]. Both INF and ETA neutralized the effects of TNFα in HeLa cells transfected with a NF-κB reporter GFP construct.…”

Section: Effect On Apoptosismentioning

confidence: 99%

“…Some authors argue that INF binds to both tmTNF as well as soluble TNFα, while ETA binds primarily to soluble TNF, and so cannot mediate caspase-dependent apoptosis [17]. Others claim that both INF and ETA bind to the uncleavable form of membrane bound TNF, but INF binds with higher avidity [18].…”

Section: Limiting Factors Contributing To Disease Restriction In Thermentioning

confidence: 99%

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TNFα blockade in human diseases: Mechanisms and future directions

Wong

Ziring

Korin

et al. 2008

Clinical Immunology

255

162

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Tumor necrosis factor-alpha (TNFα) antagonists have shown remarkable efficacy in a variety of immune-mediated inflammatory diseases (IMIDs). Therapeutic scope and limitations of these agents are reviewed in a recently published article in the Journal. In spite of their therapeutic popularity, little is known about their modes of action in vivo and factors that limit their scope of therapeutic use. Intriguingly, while all TNFα antagonists including blocking antibodies and soluble receptors are effective in certain IMIDs, only anti-TNFα antibodies are effective in other IMIDs. Early efforts at understanding how TNFα antagonists act in IMIDs centered on their ability to neutralize soluble TNFα or to block TNF receptors from binding to their ligands. Subsequent studies suggested a role of complement-mediated lysis or antibody-dependent cell cytotoxicity in their therapeutic effects. More recent models postulate that TNFα blockers may act by affecting intracellular signaling, with the end result being a hastened cell cycle arrest, apoptosis, suppression of cytokine production, or improved Treg cell function. TNFα antagonists can also modulate the functions of myofibroblasts and osteoclasts, which might explain how TNFα antagonists reduce tissue damage in chronic IMIDs. Focusing on the human therapeutic experience, this analytical review will review the biology of mechanisms of action, the limiting factors contributing to disease restriction in therapeutic efficacy, and the mechanism and frequency of treatment-limiting adverse responses of TNFα antagonists. It is hoped that the overview will address the needs of clinicians to decide on optimal use, spur clinical innovation, and incite translational researchers to set priorities for in vivo human investigations.

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Infliximab but not etanercept induces apoptosis in lamina propria T-lymphocytes from patients with Crohn’s disease

Cited by 675 publications

References 45 publications

Risk of tuberculosis is higher with anti–tumor necrosis factor monoclonal antibody therapy than with soluble tumor necrosis factor receptor therapy: The three‐year prospective french research axed on tolerance of biotherapies registry

Risk of tuberculosis is higher with anti–tumor necrosis factor monoclonal antibody therapy than with soluble tumor necrosis factor receptor therapy: The three‐year prospective french research axed on tolerance of biotherapies registry

Current and emerging therapeutic targets for IBD

TNFα blockade in human diseases: Mechanisms and future directions

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