Circulating T cells to infliximab are detectable mainly in treated patients developing anti‐drug antibodies and hypersensitivity reactions
Summary Antibodies recognizing infliximab (IFX) may develop in a proportion of treated patients, leading to loss of response or hypersensitivity reactions (HRs). T cell response to IFX has been poorly investigated. This paper was addressed to detect IFX‐specific T cells in treated patients with infl...
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Published in | Clinical and experimental immunology Vol. 186; no. 3; pp. 364 - 372 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
Oxford University Press
01.12.2016
John Wiley and Sons Inc |
Subjects | |
Online Access | Get full text |
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Abstract | Summary
Antibodies recognizing infliximab (IFX) may develop in a proportion of treated patients, leading to loss of response or hypersensitivity reactions (HRs). T cell response to IFX has been poorly investigated. This paper was addressed to detect IFX‐specific T cells in treated patients with inflammatory diseases developing, or not, anti‐drug antibodies (ADA) and to correlate the presence of specific T cells with the clinical outcomes of the treatment. A co‐culture system of IFX‐loaded dendritic cells and purified autologous CD4+ T cells was used to detect memory T cells in 32 ADA+ and 39 ADA– IFX‐treated patients and control groups. The cytokine profile of IFX‐specific T cells was also studied in culture supernatants. IFX‐specific cell proliferation was detected mainly in cells from ADA+ patients, irrespective of their different diseases. HR patients displayed higher T cell proliferation than non‐responder and tolerant patients. A mixed [interferon (IFN)‐γ, interleukin (IL)‐13, IL‐10] cytokine profile was shown in cells from ADA+ patients, while IL‐10 was the most frequently detected cytokine in the supernatants of cultures from ADA‐ patients. Immunoglobulin (Ig)E+ADA+ patients with previous HRs exhibited a more pronounced type 2 profile than IgE–ADA+ patients. This work provides evidence that IFX‐specific circulating T cells are detectable mainly in ADA+ patients with HRs, regardless of their disease. The IFX‐induced cytokine pattern partially correlates with the ADA isotype.
T cell response to IFX is detectable in a proportion of treated patients, mainly in ADA+ patients who displayed an immediate hypersensitivity reaction
The cytokine profile partially correlates with the clinical outcome of the treatment
Proliferation assay combined with cyokines evaluation may work better than the single test in evaluating cell sensitization |
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AbstractList | Summary Antibodies recognizing infliximab (IFX) may develop in a proportion of treated patients, leading to loss of response or hypersensitivity reactions (HRs). T cell response to IFX has been poorly investigated. This paper was addressed to detect IFX-specific T cells in treated patients with inflammatory diseases developing, or not, anti-drug antibodies (ADA) and to correlate the presence of specific T cells with the clinical outcomes of the treatment. A co-culture system of IFX-loaded dendritic cells and purified autologous CD4+ T cells was used to detect memory T cells in 32 ADA+ and 39 ADA- IFX-treated patients and control groups. The cytokine profile of IFX-specific T cells was also studied in culture supernatants. IFX-specific cell proliferation was detected mainly in cells from ADA+ patients, irrespective of their different diseases. HR patients displayed higher T cell proliferation than non-responder and tolerant patients. A mixed [interferon (IFN)-[gamma], interleukin (IL)-13, IL-10] cytokine profile was shown in cells from ADA+ patients, while IL-10 was the most frequently detected cytokine in the supernatants of cultures from ADA- patients. Immunoglobulin (Ig)E+ADA+ patients with previous HRs exhibited a more pronounced type 2 profile than IgE-ADA+ patients. This work provides evidence that IFX-specific circulating T cells are detectable mainly in ADA+ patients with HRs, regardless of their disease. The IFX-induced cytokine pattern partially correlates with the ADA isotype. Antibodies recognizing infliximab (IFX) may develop in a proportion of treated patients, leading to loss of response or hypersensitivity reactions (HRs). T cell response to IFX has been poorly investigated. This paper was addressed to detect IFX‐specific T cells in treated patients with inflammatory diseases developing, or not, anti‐drug antibodies (ADA) and to correlate the presence of specific T cells with the clinical outcomes of the treatment. A co‐culture system of IFX‐loaded dendritic cells and purified autologous CD4 + T cells was used to detect memory T cells in 32 ADA + and 39 ADA – IFX‐treated patients and control groups. The cytokine profile of IFX‐specific T cells was also studied in culture supernatants. IFX‐specific cell proliferation was detected mainly in cells from ADA + patients, irrespective of their different diseases. HR patients displayed higher T cell proliferation than non‐responder and tolerant patients. A mixed [interferon (IFN)‐γ, interleukin (IL)‐13, IL‐10] cytokine profile was shown in cells from ADA + patients, while IL‐10 was the most frequently detected cytokine in the supernatants of cultures from ADA‐ patients. Immunoglobulin (Ig)E + ADA + patients with previous HRs exhibited a more pronounced type 2 profile than IgE – ADA + patients. This work provides evidence that IFX‐specific circulating T cells are detectable mainly in ADA + patients with HRs, regardless of their disease. The IFX‐induced cytokine pattern partially correlates with the ADA isotype. Antibodies recognizing infliximab (IFX) may develop in a proportion of treated patients, leading to loss of response or hypersensitivity reactions (HRs). T cell response to IFX has been poorly investigated. This paper was addressed to detect IFX-specific T cells in treated patients with inflammatory diseases developing, or not, anti-drug antibodies (ADA) and to correlate the presence of specific T cells with the clinical outcomes of the treatment. A co-culture system of IFX-loaded dendritic cells and purified autologous CD4 T cells was used to detect memory T cells in 32 ADA and 39 ADA IFX-treated patients and control groups. The cytokine profile of IFX-specific T cells was also studied in culture supernatants. IFX-specific cell proliferation was detected mainly in cells from ADA patients, irrespective of their different diseases. HR patients displayed higher T cell proliferation than non-responder and tolerant patients. A mixed [interferon (IFN)-γ, interleukin (IL)-13, IL-10] cytokine profile was shown in cells from ADA patients, while IL-10 was the most frequently detected cytokine in the supernatants of cultures from ADA- patients. Immunoglobulin (Ig)E ADA patients with previous HRs exhibited a more pronounced type 2 profile than IgE ADA patients. This work provides evidence that IFX-specific circulating T cells are detectable mainly in ADA patients with HRs, regardless of their disease. The IFX-induced cytokine pattern partially correlates with the ADA isotype. Summary Antibodies recognizing infliximab (IFX) may develop in a proportion of treated patients, leading to loss of response or hypersensitivity reactions (HRs). T cell response to IFX has been poorly investigated. This paper was addressed to detect IFX‐specific T cells in treated patients with inflammatory diseases developing, or not, anti‐drug antibodies (ADA) and to correlate the presence of specific T cells with the clinical outcomes of the treatment. A co‐culture system of IFX‐loaded dendritic cells and purified autologous CD4+ T cells was used to detect memory T cells in 32 ADA+ and 39 ADA– IFX‐treated patients and control groups. The cytokine profile of IFX‐specific T cells was also studied in culture supernatants. IFX‐specific cell proliferation was detected mainly in cells from ADA+ patients, irrespective of their different diseases. HR patients displayed higher T cell proliferation than non‐responder and tolerant patients. A mixed [interferon (IFN)‐γ, interleukin (IL)‐13, IL‐10] cytokine profile was shown in cells from ADA+ patients, while IL‐10 was the most frequently detected cytokine in the supernatants of cultures from ADA‐ patients. Immunoglobulin (Ig)E+ADA+ patients with previous HRs exhibited a more pronounced type 2 profile than IgE–ADA+ patients. This work provides evidence that IFX‐specific circulating T cells are detectable mainly in ADA+ patients with HRs, regardless of their disease. The IFX‐induced cytokine pattern partially correlates with the ADA isotype. T cell response to IFX is detectable in a proportion of treated patients, mainly in ADA+ patients who displayed an immediate hypersensitivity reaction The cytokine profile partially correlates with the clinical outcome of the treatment Proliferation assay combined with cyokines evaluation may work better than the single test in evaluating cell sensitization Antibodies recognizing infliximab (IFX) may develop in a proportion of treated patients, leading to loss of response or hypersensitivity reactions (HRs). T cell response to IFX has been poorly investigated. This paper was addressed to detect IFX-specific T cells in treated patients with inflammatory diseases developing, or not, anti-drug antibodies (ADA) and to correlate the presence of specific T cells with the clinical outcomes of the treatment. A co-culture system of IFX-loaded dendritic cells and purified autologous CD4+ T cells was used to detect memory T cells in 32 ADA+ and 39 ADA- IFX-treated patients and control groups. The cytokine profile of IFX-specific T cells was also studied in culture supernatants. IFX-specific cell proliferation was detected mainly in cells from ADA+ patients, irrespective of their different diseases. HR patients displayed higher T cell proliferation than non-responder and tolerant patients. A mixed [interferon (IFN)-γ, interleukin (IL)-13, IL-10] cytokine profile was shown in cells from ADA+ patients, while IL-10 was the most frequently detected cytokine in the supernatants of cultures from ADA- patients. Immunoglobulin (Ig)E+ ADA+ patients with previous HRs exhibited a more pronounced type 2 profile than IgE- ADA+ patients. This work provides evidence that IFX-specific circulating T cells are detectable mainly in ADA+ patients with HRs, regardless of their disease. The IFX-induced cytokine pattern partially correlates with the ADA isotype.Antibodies recognizing infliximab (IFX) may develop in a proportion of treated patients, leading to loss of response or hypersensitivity reactions (HRs). T cell response to IFX has been poorly investigated. This paper was addressed to detect IFX-specific T cells in treated patients with inflammatory diseases developing, or not, anti-drug antibodies (ADA) and to correlate the presence of specific T cells with the clinical outcomes of the treatment. A co-culture system of IFX-loaded dendritic cells and purified autologous CD4+ T cells was used to detect memory T cells in 32 ADA+ and 39 ADA- IFX-treated patients and control groups. The cytokine profile of IFX-specific T cells was also studied in culture supernatants. IFX-specific cell proliferation was detected mainly in cells from ADA+ patients, irrespective of their different diseases. HR patients displayed higher T cell proliferation than non-responder and tolerant patients. A mixed [interferon (IFN)-γ, interleukin (IL)-13, IL-10] cytokine profile was shown in cells from ADA+ patients, while IL-10 was the most frequently detected cytokine in the supernatants of cultures from ADA- patients. Immunoglobulin (Ig)E+ ADA+ patients with previous HRs exhibited a more pronounced type 2 profile than IgE- ADA+ patients. This work provides evidence that IFX-specific circulating T cells are detectable mainly in ADA+ patients with HRs, regardless of their disease. The IFX-induced cytokine pattern partially correlates with the ADA isotype. Antibodies recognizing infliximab (IFX) may develop in a proportion of treated patients, leading to loss of response or hypersensitivity reactions (HRs). T cell response to IFX has been poorly investigated. This paper was addressed to detect IFX-specific T cells in treated patients with inflammatory diseases developing, or not, anti-drug antibodies (ADA) and to correlate the presence of specific T cells with the clinical outcomes of the treatment. A co-culture system of IFX-loaded dendritic cells and purified autologous CD4+ T cells was used to detect memory T cells in 32 ADA+ and 39 ADA– IFX-treated patients and control groups. The cytokine profile of IFX-specific T cells was also studied in culture supernatants. IFX-specific cell proliferation was detected mainly in cells from ADA+ patients, irrespective of their different diseases. HR patients displayed higher T cell proliferation than non-responder and tolerant patients. A mixed [interferon (IFN)-γ, interleukin (IL)-13, IL-10] cytokine profile was shown in cells from ADA+ patients, while IL-10 was the most frequently detected cytokine in the supernatants of cultures from ADA- patients. Immunoglobulin (Ig)E+ADA+ patients with previous HRs exhibited a more pronounced type 2 profile than IgE–ADA+ patients. This work provides evidence that IFX-specific circulating T cells are detectable mainly in ADA+ patients with HRs, regardless of their disease. The IFX-induced cytokine pattern partially correlates with the ADA isotype. Antibodies recognizing infliximab (IFX) may develop in a proportion of treated patients, leading to loss of response or hypersensitivity reactions (HRs). T cell response to IFX has been poorly investigated. This paper was addressed to detect IFX-specific T cells in treated patients with inflammatory diseases developing, or not, anti-drug antibodies (ADA) and to correlate the presence of specific T cells with the clinical outcomes of the treatment. A co-culture system of IFX-loaded dendritic cells and purified autologous CD4 super(+) T cells was used to detect memory T cells in 32 ADA super(+) and 39 ADA super(-) IFX-treated patients and control groups. The cytokine profile of IFX-specific T cells was also studied in culture supernatants. IFX-specific cell proliferation was detected mainly in cells from ADA super(+) patients, irrespective of their different diseases. HR patients displayed higher T cell proliferation than non-responder and tolerant patients. A mixed [interferon (IFN)- gamma , interleukin (IL)-13, IL-10] cytokine profile was shown in cells from ADA super(+) patients, while IL-10 was the most frequently detected cytokine in the supernatants of cultures from ADA- patients. Immunoglobulin (Ig)E super(+)ADA super(+) patients with previous HRs exhibited a more pronounced type 2 profile than IgE super(-)ADA super(+) patients. This work provides evidence that IFX-specific circulating T cells are detectable mainly in ADA super(+) patients with HRs, regardless of their disease. The IFX-induced cytokine pattern partially correlates with the ADA isotype. * T cell response to IFX is detectable in a proportion of treated patients, mainly in ADA+ patients who displayed an immediate hypersensitivity reaction * The cytokine profile partially correlates with the clinical outcome of the treatment * Proliferation assay combined with cyokines evaluation may work better than the single test in evaluating cell sensitization |
Author | Milla, M. Pratesi, S. Prignano, F. Nencini, F. Annese, V. Romagnani, S. Maggi, E. Matucci, A. Vultaggio, A. Petroni, G. Cammelli, D. |
AuthorAffiliation | 1 Centre of Research DENOTHE and Department of Experimental and Clinical Medicine University of Florence Italy 4 Dermatology Clinic, Azienda Sanitaria Firenze, Department of Surgery and Translational Medicine University of Florence Florence Italy 3 Gastroenterology Unit Azienda Ospedaliero‐Universitaria Careggi Florence Italy 2 Immunoallergology Unit Azienda Ospedaliero‐Universitaria Careggi Florence Italy |
AuthorAffiliation_xml | – name: 4 Dermatology Clinic, Azienda Sanitaria Firenze, Department of Surgery and Translational Medicine University of Florence Florence Italy – name: 1 Centre of Research DENOTHE and Department of Experimental and Clinical Medicine University of Florence Italy – name: 2 Immunoallergology Unit Azienda Ospedaliero‐Universitaria Careggi Florence Italy – name: 3 Gastroenterology Unit Azienda Ospedaliero‐Universitaria Careggi Florence Italy |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27569750$$D View this record in MEDLINE/PubMed |
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Cites_doi | 10.1053/j.gastro.2010.10.008 10.1038/nrrheum.2013.4 10.1093/rheumatology/keq031 10.1016/j.berh.2014.10.019 10.1136/gut.2009.201533 10.1111/cea.12098 10.2165/00003495-200565150-00014 10.1016/S0140-6736(80)92767-1 10.1159/000336839 10.3899/jrheum.091464 10.1136/ard.2009.110502 10.1016/j.jaci.2004.04.029 10.1016/j.jpba.2008.09.020 10.1002/ibd.20520 10.1016/j.cyto.2008.11.008 10.1586/eci.10.90 10.1002/art.23200 10.1016/j.clim.2014.02.008 10.1016/j.trsl.2014.09.006 10.1136/ard.62.9.817 10.1111/j.1398-9995.2009.02280.x 10.1053/j.gastro.2004.11.060 10.1096/fj.10-173872 10.1136/ard.2008.101279 10.1038/ncomms4199 10.1002/art.23447 |
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References | 2009; 45 2009; 68 2013; 43 2011; 60 2015; 165 2008; 58 2008; 14 2005; 65 2014; 151 2014; 28 2010; 85 2005; 23 2011; 7 2013; 9 2010; 65 2010; 49 2014; 5 2004; 114 2010; 69 1980; 1 2005; 128 2008; 48 2011; 25 2012; 159 2011; 140 2003; 62 Matucci (2021120807481525800_cei12858-bib-0008) 2013; 43 Fransen (2021120807481525800_cei12858-bib-0014) 2005; 23 Braun (2021120807481525800_cei12858-bib-0015) 2003; 62 Lewis (2021120807481525800_cei12858-bib-0012) 2008; 14 van Schouwenburg (2021120807481525800_cei12858-bib-0004) 2013; 9 Delluc (2021120807481525800_cei12858-bib-0010) 2011; 25 Vultaggio (2021120807481525800_cei12858-bib-0021) 2012; 159 Mitoma (2021120807481525800_cei12858-bib-0005) 2008; 58 Shankar (2021120807481525800_cei12858-bib-0017) 2008; 48 Boks (2021120807481525800_cei12858-bib-0023) 2014; 151 Arora (2021120807481525800_cei12858-bib-0006) 2009; 45 Vos (2021120807481525800_cei12858-bib-0024) 2011; 140 Vultaggio (2021120807481525800_cei12858-bib-0018) 2010; 65 Bressler (2021120807481525800_cei12858-bib-0002) 2010; 85 Van den Bosch (2021120807481525800_cei12858-bib-0019) 2014; 28 Belostocki (2021120807481525800_cei12858-bib-0027) 2008; 58 Baldwin (2021120807481525800_cei12858-bib-0026) 2010; 69 Siddiqui (2021120807481525800_cei12858-bib-0003) 2005; 65 Mitoma (2021120807481525800_cei12858-bib-0025) 2005; 128 Brown (2021120807481525800_cei12858-bib-0011) 2004; 114 Mukhtyar (2021120807481525800_cei12858-bib-0016) 2009; 68 Willrich (2021120807481525800_cei12858-bib-0001) 2015; 165 Ben-Horin (2021120807481525800_cei12858-bib-0009) 2011; 60 Harvey (2021120807481525800_cei12858-bib-0013) 1980; 1 Maggi (2021120807481525800_cei12858-bib-0020) 2011; 7 Evans (2021120807481525800_cei12858-bib-0022) 2014; 5 Horiuchi (2021120807481525800_cei12858-bib-0007) 2010; 49 21162650 - Expert Rev Clin Immunol. 2011 Jan;7(1):55-63 20194223 - Rheumatology (Oxford). 2010 Jul;49(7):1215-28 22846615 - Int Arch Allergy Immunol. 2012;159(3):321-6 21368101 - FASEB J. 2011 Jun;25(6):2040-8 20436164 - J Rheumatol Suppl. 2010 May;85:40-52 19951375 - Allergy. 2010 May;65(5):657-61 16273792 - Clin Exp Rheumatol. 2005 Sep-Oct;23(5 Suppl 39):S93-9 18623174 - Inflamm Bowel Dis. 2008 Dec;14(12):1660-6 12922952 - Ann Rheum Dis. 2003 Sep;62(9):817-24 15316518 - J Allergy Clin Immunol. 2004 Aug;114(2):371-6 18240208 - Arthritis Rheum. 2008 Feb;58(2):384-8 23711128 - Clin Exp Allergy. 2013 Jun;43(6):659-64 15685549 - Gastroenterology. 2005 Feb;128(2):376-92 25305470 - Transl Res. 2015 Feb;165(2):270-82 19054820 - Ann Rheum Dis. 2009 Dec;68(12):1827-32 24568737 - Clin Immunol. 2014 Apr;151(2):136-45 18993008 - J Pharm Biomed Anal. 2008 Dec 15;48(5):1267-81 23399692 - Nat Rev Rheumatol. 2013 Mar;9(3):164-72 6102236 - Lancet. 1980 Mar 8;1(8167):514 25488787 - Best Pract Res Clin Rheumatol. 2014 Oct;28(5):819-27 19773288 - Ann Rheum Dis. 2010 Jun;69(6):1200-7 16225377 - Drugs. 2005;65(15):2179-208 24492460 - Nat Commun. 2014;5:3199 18438840 - Arthritis Rheum. 2008 May;58(5):1248-57 20955706 - Gastroenterology. 2011 Jan;140(1):221-30 20519742 - Gut. 2011 Jan;60(1):41-8 19128982 - Cytokine. 2009 Feb;45(2):124-31 |
References_xml | – volume: 62 start-page: 817 year: 2003 end-page: 24 article-title: International ASAS consensus statement for the use of anti‐tumour necrosis factor agents in patients with ankylosing spondylitis publication-title: Ann Rheum Dis – volume: 45 start-page: 124 year: 2009 end-page: 31 article-title: Differences in binding and effector functions between classes of TNF antagonists publication-title: Cytokine – volume: 140 start-page: 221 year: 2011 end-page: 30 article-title: Anti‐tumor necrosis factor‐α antibodies induce regulatory macrophages in an Fc region‐dependent manner publication-title: Gastroenterology – volume: 5 start-page: 3199 year: 2014 article-title: TNF‐α blockade induces IL‐10 expression in human CD4+ T cells publication-title: Nat Commun – volume: 43 start-page: 659 year: 2013 end-page: 64 article-title: Allergological and evaluation of patients with hypersensitivity reactions to infliximab publication-title: Clin Exp Allergy – volume: 14 start-page: 1660 year: 2008 end-page: 6 article-title: Use of the noninvasive components of the Mayo score to assess clinical response in ulcerative colitis publication-title: Inflamm Bowel Dis – volume: 85 start-page: 40 year: 2010 end-page: 52 article-title: Optimizing use of tumor necrosis factor inhibitors in the management of immune‐mediated inflammatory diseases publication-title: J Rheumatol Suppl – volume: 1 start-page: 514 year: 1980 article-title: A simple index of Crohn's disease activity publication-title: Lancet – volume: 114 start-page: 371 year: 2004 end-page: 6 article-title: Clinical features and severity grading of anaphylaxis publication-title: J Allergy Clin Immunol – volume: 165 start-page: 270 year: 2015 end-page: 82 article-title: Tumor necrosis factor inhibitors: clinical utility in autoimmune diseases publication-title: Transl Res – volume: 151 start-page: 136 year: 2014 end-page: 45 article-title: Inhibition of TNF receptor signaling by anti‐TNFα biologicals primes naïve CD4(+) T cells towards IL‐10(+) T cells with a regulatory phenotype and function publication-title: Clin Immunol – volume: 58 start-page: 1248 year: 2008 end-page: 57 article-title: Mechanisms for cytotoxic effects of anti‐tumor necrosis factor agents on transmembrane tumor necrosis factor alpha‐expressing cells: comparison among infliximab, etanercept, and adalimumab publication-title: Arthritis Rheum – volume: 159 start-page: 321 year: 2012 end-page: 6 article-title: Drug‐specific Th2 cells and IgE antibodies in a patient with anaphylaxis to rituximab publication-title: Int Arch Allergy Immunol – volume: 48 start-page: 1267 year: 2008 end-page: 81 article-title: Recommendations for the validation of immunoassays used for detection of host antibodies against biotechnology products publication-title: J Pharm Biomed Anal – volume: 69 start-page: 1200 year: 2010 end-page: 7 article-title: Tumour necrosis factor alpha blockade impairs dendritic cell survival and function in rheumatoid arthritis publication-title: Ann Rheum Dis – volume: 128 start-page: 376 year: 2005 end-page: 92 article-title: Infliximab induces potent anti‐inflammatory responses by outside‐to‐inside signals through transmembrane TNF‐alpha publication-title: Gastroenterology – volume: 65 start-page: 657 year: 2010 end-page: 61 article-title: Anti‐infliximab IgE and non‐IgE antibodies and induction of infusion‐related severe anaphylactic reactions publication-title: Allergy – volume: 7 start-page: 55 year: 2011 end-page: 63 article-title: Acute infusion reactions induced by monoclonal antibody therapy publication-title: Expert Rev Clin Immunol – volume: 25 start-page: 2040 year: 2011 end-page: 8 article-title: Quantitative analysis of the CD4 T‐cell repertoire specific to therapeutic antibodies in healthy donors publication-title: FASEB J – volume: 28 start-page: 819 year: 2014 end-page: 27 article-title: Treatment of spondyloarthritis beyond TNF‐alpha blockade publication-title: Best Pract Res Clin Rheumatol – volume: 23 start-page: S93 year: 2005 end-page: 9 article-title: The Disease Activity Score and the EULAR response criteria publication-title: Clin Exp Rheumatol – volume: 49 start-page: 1215 year: 2010 end-page: 8 article-title: Transmembrane TNF‐alpha: structure, function and interaction with anti‐TNF agents publication-title: Rheumatology (Oxf) – volume: 58 start-page: 384 year: 2008 end-page: 8 article-title: Infliximab treatment shifts the balance between stimulatory and inhibitory Fcgamma receptor type II isoforms on neutrophils in patients with rheumatoid arthritis publication-title: Arthritis Rheum – volume: 68 start-page: 1827 year: 2009 end-page: 32 article-title: Modification and validation of the Birmingham Vasculitis Activity Score (version 3) publication-title: Ann Rheum Dis – volume: 9 start-page: 164 year: 2013 end-page: 72 article-title: Immunogenicity of anti‐TNF biologic therapies for rheumatoid arthritis publication-title: Nat Rev Rheumatol – volume: 65 start-page: 2179 year: 2005 end-page: 88 article-title: Infliximab: a review of its use in Crohn's disease and rheumatoid arthritis publication-title: Drugs – volume: 60 start-page: 41 year: 2011 end-page: 8 article-title: The immunogenic part of infliximab is the F(ab)2, but measuring antibodies to the intact infliximab molecule is more clinically useful publication-title: Gut – volume: 140 start-page: 221 year: 2011 ident: 2021120807481525800_cei12858-bib-0024 article-title: Anti-tumor necrosis factor-α antibodies induce regulatory macrophages in an Fc region-dependent manner publication-title: Gastroenterology doi: 10.1053/j.gastro.2010.10.008 – volume: 9 start-page: 164 year: 2013 ident: 2021120807481525800_cei12858-bib-0004 article-title: Immunogenicity of anti-TNF biologic therapies for rheumatoid arthritis publication-title: Nat Rev Rheumatol doi: 10.1038/nrrheum.2013.4 – volume: 49 start-page: 1215 year: 2010 ident: 2021120807481525800_cei12858-bib-0007 article-title: Transmembrane TNF-alpha: structure, function and interaction with anti-TNF agents publication-title: Rheumatology (Oxf) doi: 10.1093/rheumatology/keq031 – volume: 28 start-page: 819 year: 2014 ident: 2021120807481525800_cei12858-bib-0019 article-title: Treatment of spondyloarthritis beyond TNF-alpha blockade publication-title: Best Pract Res Clin Rheumatol doi: 10.1016/j.berh.2014.10.019 – volume: 60 start-page: 41 year: 2011 ident: 2021120807481525800_cei12858-bib-0009 article-title: The immunogenic part of infliximab is the F(ab)2, but measuring antibodies to the intact infliximab molecule is more clinically useful publication-title: Gut doi: 10.1136/gut.2009.201533 – volume: 23 start-page: S93 year: 2005 ident: 2021120807481525800_cei12858-bib-0014 article-title: The Disease Activity Score and the EULAR response criteria publication-title: Clin Exp Rheumatol – volume: 43 start-page: 659 year: 2013 ident: 2021120807481525800_cei12858-bib-0008 article-title: Allergological in vitro and in vivo evaluation of patients with hypersensitivity reactions to infliximab publication-title: Clin Exp Allergy doi: 10.1111/cea.12098 – volume: 65 start-page: 2179 year: 2005 ident: 2021120807481525800_cei12858-bib-0003 article-title: Infliximab: a review of its use in Crohn's disease and rheumatoid arthritis publication-title: Drugs doi: 10.2165/00003495-200565150-00014 – volume: 1 start-page: 514 year: 1980 ident: 2021120807481525800_cei12858-bib-0013 article-title: A simple index of Crohn's disease activity publication-title: Lancet doi: 10.1016/S0140-6736(80)92767-1 – volume: 159 start-page: 321 year: 2012 ident: 2021120807481525800_cei12858-bib-0021 article-title: Drug-specific Th2 cells and IgE antibodies in a patient with anaphylaxis to rituximab publication-title: Int Arch Allergy Immunol doi: 10.1159/000336839 – volume: 85 start-page: 40 year: 2010 ident: 2021120807481525800_cei12858-bib-0002 article-title: Optimizing use of tumor necrosis factor inhibitors in the management of immune-mediated inflammatory diseases publication-title: J Rheumatol Suppl doi: 10.3899/jrheum.091464 – volume: 69 start-page: 1200 year: 2010 ident: 2021120807481525800_cei12858-bib-0026 article-title: Tumour necrosis factor alpha blockade impairs dendritic cell survival and function in rheumatoid arthritis publication-title: Ann Rheum Dis doi: 10.1136/ard.2009.110502 – volume: 114 start-page: 371 year: 2004 ident: 2021120807481525800_cei12858-bib-0011 article-title: Clinical features and severity grading of anaphylaxis publication-title: J Allergy Clin Immunol doi: 10.1016/j.jaci.2004.04.029 – volume: 48 start-page: 1267 year: 2008 ident: 2021120807481525800_cei12858-bib-0017 article-title: Recommendations for the validation of immunoassays used for detection of host antibodies against biotechnology products publication-title: J Pharm Biomed Anal doi: 10.1016/j.jpba.2008.09.020 – volume: 14 start-page: 1660 year: 2008 ident: 2021120807481525800_cei12858-bib-0012 article-title: Use of the noninvasive components of the Mayo score to assess clinical response in ulcerative colitis publication-title: Inflamm Bowel Dis doi: 10.1002/ibd.20520 – volume: 45 start-page: 124 year: 2009 ident: 2021120807481525800_cei12858-bib-0006 article-title: Differences in binding and effector functions between classes of TNF antagonists publication-title: Cytokine doi: 10.1016/j.cyto.2008.11.008 – volume: 7 start-page: 55 year: 2011 ident: 2021120807481525800_cei12858-bib-0020 article-title: Acute infusion reactions induced by monoclonal antibody therapy publication-title: Expert Rev Clin Immunol doi: 10.1586/eci.10.90 – volume: 58 start-page: 384 year: 2008 ident: 2021120807481525800_cei12858-bib-0027 article-title: Infliximab treatment shifts the balance between stimulatory and inhibitory Fcgamma receptor type II isoforms on neutrophils in patients with rheumatoid arthritis publication-title: Arthritis Rheum doi: 10.1002/art.23200 – volume: 151 start-page: 136 year: 2014 ident: 2021120807481525800_cei12858-bib-0023 article-title: Inhibition of TNF receptor signaling by anti-TNFα biologicals primes naïve CD4(+) T cells towards IL-10(+) T cells with a regulatory phenotype and function publication-title: Clin Immunol doi: 10.1016/j.clim.2014.02.008 – volume: 165 start-page: 270 year: 2015 ident: 2021120807481525800_cei12858-bib-0001 article-title: Tumor necrosis factor inhibitors: clinical utility in autoimmune diseases publication-title: Transl Res doi: 10.1016/j.trsl.2014.09.006 – volume: 62 start-page: 817 year: 2003 ident: 2021120807481525800_cei12858-bib-0015 article-title: International ASAS consensus statement for the use of anti-tumour necrosis factor agents in patients with ankylosing spondylitis publication-title: Ann Rheum Dis doi: 10.1136/ard.62.9.817 – volume: 65 start-page: 657 year: 2010 ident: 2021120807481525800_cei12858-bib-0018 article-title: Anti-infliximab IgE and non-IgE antibodies and induction of infusion-related severe anaphylactic reactions publication-title: Allergy doi: 10.1111/j.1398-9995.2009.02280.x – volume: 128 start-page: 376 year: 2005 ident: 2021120807481525800_cei12858-bib-0025 article-title: Infliximab induces potent anti-inflammatory responses by outside-to-inside signals through transmembrane TNF-alpha publication-title: Gastroenterology doi: 10.1053/j.gastro.2004.11.060 – volume: 25 start-page: 2040 year: 2011 ident: 2021120807481525800_cei12858-bib-0010 article-title: Quantitative analysis of the CD4 T-cell repertoire specific to therapeutic antibodies in healthy donors publication-title: FASEB J doi: 10.1096/fj.10-173872 – volume: 68 start-page: 1827 year: 2009 ident: 2021120807481525800_cei12858-bib-0016 article-title: Modification and validation of the Birmingham Vasculitis Activity Score (version 3) publication-title: Ann Rheum Dis doi: 10.1136/ard.2008.101279 – volume: 5 start-page: 3199 year: 2014 ident: 2021120807481525800_cei12858-bib-0022 article-title: TNF-α blockade induces IL-10 expression in human CD4+ T cells publication-title: Nat Commun doi: 10.1038/ncomms4199 – volume: 58 start-page: 1248 year: 2008 ident: 2021120807481525800_cei12858-bib-0005 article-title: Mechanisms for cytotoxic effects of anti-tumor necrosis factor agents on transmembrane tumor necrosis factor alpha-expressing cells: comparison among infliximab, etanercept, and adalimumab publication-title: Arthritis Rheum doi: 10.1002/art.23447 – reference: 19951375 - Allergy. 2010 May;65(5):657-61 – reference: 22846615 - Int Arch Allergy Immunol. 2012;159(3):321-6 – reference: 20436164 - J Rheumatol Suppl. 2010 May;85:40-52 – reference: 19773288 - Ann Rheum Dis. 2010 Jun;69(6):1200-7 – reference: 16273792 - Clin Exp Rheumatol. 2005 Sep-Oct;23(5 Suppl 39):S93-9 – reference: 25488787 - Best Pract Res Clin Rheumatol. 2014 Oct;28(5):819-27 – reference: 18993008 - J Pharm Biomed Anal. 2008 Dec 15;48(5):1267-81 – reference: 19054820 - Ann Rheum Dis. 2009 Dec;68(12):1827-32 – reference: 20519742 - Gut. 2011 Jan;60(1):41-8 – reference: 12922952 - Ann Rheum Dis. 2003 Sep;62(9):817-24 – reference: 18438840 - Arthritis Rheum. 2008 May;58(5):1248-57 – reference: 24568737 - Clin Immunol. 2014 Apr;151(2):136-45 – reference: 21162650 - Expert Rev Clin Immunol. 2011 Jan;7(1):55-63 – reference: 20194223 - Rheumatology (Oxford). 2010 Jul;49(7):1215-28 – reference: 24492460 - Nat Commun. 2014;5:3199 – reference: 18623174 - Inflamm Bowel Dis. 2008 Dec;14(12):1660-6 – reference: 23399692 - Nat Rev Rheumatol. 2013 Mar;9(3):164-72 – reference: 16225377 - Drugs. 2005;65(15):2179-208 – reference: 21368101 - FASEB J. 2011 Jun;25(6):2040-8 – reference: 18240208 - Arthritis Rheum. 2008 Feb;58(2):384-8 – reference: 25305470 - Transl Res. 2015 Feb;165(2):270-82 – reference: 6102236 - Lancet. 1980 Mar 8;1(8167):514 – reference: 15316518 - J Allergy Clin Immunol. 2004 Aug;114(2):371-6 – reference: 20955706 - Gastroenterology. 2011 Jan;140(1):221-30 – reference: 23711128 - Clin Exp Allergy. 2013 Jun;43(6):659-64 – reference: 15685549 - Gastroenterology. 2005 Feb;128(2):376-92 – reference: 19128982 - Cytokine. 2009 Feb;45(2):124-31 |
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Antibodies recognizing infliximab (IFX) may develop in a proportion of treated patients, leading to loss of response or hypersensitivity reactions... Antibodies recognizing infliximab (IFX) may develop in a proportion of treated patients, leading to loss of response or hypersensitivity reactions (HRs). T... Summary Antibodies recognizing infliximab (IFX) may develop in a proportion of treated patients, leading to loss of response or hypersensitivity reactions... |
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SubjectTerms | Adult Aged allergy Antirheumatic Agents - adverse effects arthritis Cell growth Cytokines Cytokines - metabolism Drug Hypersensitivity - blood Drug Hypersensitivity - immunology Female Humans Immune System Diseases - complications Immune System Diseases - drug therapy Immune System Diseases - immunology Immunoglobulin E - immunology Immunoglobulins Infliximab - adverse effects Infliximab - therapeutic use Isoantibodies - blood Isoantibodies - immunology Lymphocyte Activation - immunology Lymphocyte Count Lymphocytes Male Middle Aged Original T cells T-Lymphocyte Subsets - immunology T-Lymphocyte Subsets - metabolism |
Title | Circulating T cells to infliximab are detectable mainly in treated patients developing anti‐drug antibodies and hypersensitivity reactions |
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