Immunogenicity to biological drugs in psoriasis and psoriatic arthritis

Detalhes bibliográficos
Autor(a) principal: Valenzuela, Fernando
Data de Publicação: 2021
Outros Autores: Flores, Rodrigo
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Clinics
Texto Completo: https://www.revistas.usp.br/clinics/article/view/213021
Resumo: Monoclonal antibodies or fusion proteins, defined as biological drugs, have modified the natural history of numerous immune-mediated disorders, allowing the development of therapies aimed at blocking the pathophysiological pathways of the disease, providing greater efficacy and safety than conventional treatment strategies. Virtually all therapeutic proteins elicit an immune response, producing anti-drug antibodies (ADAs) against hypervariable regions of immunoglobulins. Immunogenicity against biological drugs can alter their pharmacokinetic and pharmacodynamic properties, thereby reducing the efficacy of these drugs. In more severe cases, ADAs can neutralize the therapeutic effects of the drug or cause serious adverse effects, mainly hypersensitivity reactions. The prevalence of ADAs varies widely depending on the type of test used, occurrence of false-negative results, and non-specific binding to the drug, making it difficult to accurately assess their clinical impact. Concomitant use of immunosuppressors efficiently reduces the immunogenicity in a dose-dependent manner, either by decreasing the frequency of detectable ADAs or by delaying their appearance, thereby enhancing the effectiveness of biological therapies. Among the new therapeutic strategies for the management of psoriasis, biological agents have gained increasing importance in recent years as they interrupt key inflammation pathways involved in the physiopathology of the disease. Reports regarding ADA in new biologics are still scarce, but the most recent evidence tends to show little impact on the clinical response to the drug, even with prolonged treatment. It is therefore essential to standardize laboratory tests to determine the presence and titles of ADAs to establish their administration and management guidelines that allow the determination of the real clinical impact of these drugs.
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spelling Immunogenicity to biological drugs in psoriasis and psoriatic arthritisImmunogenicityAnti-Drug AntibodiesAnti-TNFAnti-IL-12/23Anti-IL-17Anti-IL-23Monoclonal antibodies or fusion proteins, defined as biological drugs, have modified the natural history of numerous immune-mediated disorders, allowing the development of therapies aimed at blocking the pathophysiological pathways of the disease, providing greater efficacy and safety than conventional treatment strategies. Virtually all therapeutic proteins elicit an immune response, producing anti-drug antibodies (ADAs) against hypervariable regions of immunoglobulins. Immunogenicity against biological drugs can alter their pharmacokinetic and pharmacodynamic properties, thereby reducing the efficacy of these drugs. In more severe cases, ADAs can neutralize the therapeutic effects of the drug or cause serious adverse effects, mainly hypersensitivity reactions. The prevalence of ADAs varies widely depending on the type of test used, occurrence of false-negative results, and non-specific binding to the drug, making it difficult to accurately assess their clinical impact. Concomitant use of immunosuppressors efficiently reduces the immunogenicity in a dose-dependent manner, either by decreasing the frequency of detectable ADAs or by delaying their appearance, thereby enhancing the effectiveness of biological therapies. Among the new therapeutic strategies for the management of psoriasis, biological agents have gained increasing importance in recent years as they interrupt key inflammation pathways involved in the physiopathology of the disease. Reports regarding ADA in new biologics are still scarce, but the most recent evidence tends to show little impact on the clinical response to the drug, even with prolonged treatment. It is therefore essential to standardize laboratory tests to determine the presence and titles of ADAs to establish their administration and management guidelines that allow the determination of the real clinical impact of these drugs.Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo2021-10-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://www.revistas.usp.br/clinics/article/view/21302110.6061/clinics/2021/e3015Clinics; Vol. 76 (2021); e3015Clinics; v. 76 (2021); e3015Clinics; Vol. 76 (2021); e30151980-53221807-5932reponame:Clinicsinstname:Universidade de São Paulo (USP)instacron:USPenghttps://www.revistas.usp.br/clinics/article/view/213021/195037Copyright (c) 2023 Clinicsinfo:eu-repo/semantics/openAccessValenzuela, FernandoFlores, Rodrigo2023-07-06T13:04:10Zoai:revistas.usp.br:article/213021Revistahttps://www.revistas.usp.br/clinicsPUBhttps://www.revistas.usp.br/clinics/oai||clinics@hc.fm.usp.br1980-53221807-5932opendoar:2023-07-06T13:04:10Clinics - Universidade de São Paulo (USP)false
dc.title.none.fl_str_mv Immunogenicity to biological drugs in psoriasis and psoriatic arthritis
title Immunogenicity to biological drugs in psoriasis and psoriatic arthritis
spellingShingle Immunogenicity to biological drugs in psoriasis and psoriatic arthritis
Valenzuela, Fernando
Immunogenicity
Anti-Drug Antibodies
Anti-TNF
Anti-IL-12/23
Anti-IL-17
Anti-IL-23
title_short Immunogenicity to biological drugs in psoriasis and psoriatic arthritis
title_full Immunogenicity to biological drugs in psoriasis and psoriatic arthritis
title_fullStr Immunogenicity to biological drugs in psoriasis and psoriatic arthritis
title_full_unstemmed Immunogenicity to biological drugs in psoriasis and psoriatic arthritis
title_sort Immunogenicity to biological drugs in psoriasis and psoriatic arthritis
author Valenzuela, Fernando
author_facet Valenzuela, Fernando
Flores, Rodrigo
author_role author
author2 Flores, Rodrigo
author2_role author
dc.contributor.author.fl_str_mv Valenzuela, Fernando
Flores, Rodrigo
dc.subject.por.fl_str_mv Immunogenicity
Anti-Drug Antibodies
Anti-TNF
Anti-IL-12/23
Anti-IL-17
Anti-IL-23
topic Immunogenicity
Anti-Drug Antibodies
Anti-TNF
Anti-IL-12/23
Anti-IL-17
Anti-IL-23
description Monoclonal antibodies or fusion proteins, defined as biological drugs, have modified the natural history of numerous immune-mediated disorders, allowing the development of therapies aimed at blocking the pathophysiological pathways of the disease, providing greater efficacy and safety than conventional treatment strategies. Virtually all therapeutic proteins elicit an immune response, producing anti-drug antibodies (ADAs) against hypervariable regions of immunoglobulins. Immunogenicity against biological drugs can alter their pharmacokinetic and pharmacodynamic properties, thereby reducing the efficacy of these drugs. In more severe cases, ADAs can neutralize the therapeutic effects of the drug or cause serious adverse effects, mainly hypersensitivity reactions. The prevalence of ADAs varies widely depending on the type of test used, occurrence of false-negative results, and non-specific binding to the drug, making it difficult to accurately assess their clinical impact. Concomitant use of immunosuppressors efficiently reduces the immunogenicity in a dose-dependent manner, either by decreasing the frequency of detectable ADAs or by delaying their appearance, thereby enhancing the effectiveness of biological therapies. Among the new therapeutic strategies for the management of psoriasis, biological agents have gained increasing importance in recent years as they interrupt key inflammation pathways involved in the physiopathology of the disease. Reports regarding ADA in new biologics are still scarce, but the most recent evidence tends to show little impact on the clinical response to the drug, even with prolonged treatment. It is therefore essential to standardize laboratory tests to determine the presence and titles of ADAs to establish their administration and management guidelines that allow the determination of the real clinical impact of these drugs.
publishDate 2021
dc.date.none.fl_str_mv 2021-10-01
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv https://www.revistas.usp.br/clinics/article/view/213021
10.6061/clinics/2021/e3015
url https://www.revistas.usp.br/clinics/article/view/213021
identifier_str_mv 10.6061/clinics/2021/e3015
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv https://www.revistas.usp.br/clinics/article/view/213021/195037
dc.rights.driver.fl_str_mv Copyright (c) 2023 Clinics
info:eu-repo/semantics/openAccess
rights_invalid_str_mv Copyright (c) 2023 Clinics
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
dc.source.none.fl_str_mv Clinics; Vol. 76 (2021); e3015
Clinics; v. 76 (2021); e3015
Clinics; Vol. 76 (2021); e3015
1980-5322
1807-5932
reponame:Clinics
instname:Universidade de São Paulo (USP)
instacron:USP
instname_str Universidade de São Paulo (USP)
instacron_str USP
institution USP
reponame_str Clinics
collection Clinics
repository.name.fl_str_mv Clinics - Universidade de São Paulo (USP)
repository.mail.fl_str_mv ||clinics@hc.fm.usp.br
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