Immunosuppressive drugs modes of action

The innate and adaptive immune systems work as a complex interplay between different cell types, involving cytokines and chemokines mediating extracellular and paracrine effects. At the intracellular level, the inflammatory cascade is mediated by multifaceted processes that have been better describe...

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Published inBaillière's best practice & research. Clinical gastroenterology Vol. 54-55; p. 101757
Main Authors Meneghini, Maria, Bestard, Oriol, Grinyo, Josep Maria
Format Journal Article
LanguageEnglish
Published Kidlington Elsevier Ltd 01.10.2021
Elsevier Limited
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ISSN1521-6918
1532-1916
1532-1916
DOI10.1016/j.bpg.2021.101757

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Abstract The innate and adaptive immune systems work as a complex interplay between different cell types, involving cytokines and chemokines mediating extracellular and paracrine effects. At the intracellular level, the inflammatory cascade is mediated by multifaceted processes that have been better described in the last 10 years. Immunosuppressive agents available in clinical practice act at different points of those cascades at the intracellular or extracellular level. Those drugs can mediate their effects on one or more cell types finally limiting inflammation and immune responses to antigens. Every immunosuppressive agent is characterized by intrinsic toxicity and side effects that may be due to the same therapeutic pathways or to off-target secondary effect of each molecule. We will here review the mechanisms of action of the most widely used immunosuppressive agents in the field of solid organ transplantation and autoimmune disorders, describing the mechanisms underlying both the therapeutic and secondary effects.
AbstractList The innate and adaptive immune systems work as a complex interplay between different cell types, involving cytokines and chemokines mediating extracellular and paracrine effects. At the intracellular level, the inflammatory cascade is mediated by multifaceted processes that have been better described in the last 10 years. Immunosuppressive agents available in clinical practice act at different points of those cascades at the intracellular or extracellular level. Those drugs can mediate their effects on one or more cell types finally limiting inflammation and immune responses to antigens. Every immunosuppressive agent is characterized by intrinsic toxicity and side effects that may be due to the same therapeutic pathways or to off-target secondary effect of each molecule. We will here review the mechanisms of action of the most widely used immunosuppressive agents in the field of solid organ transplantation and autoimmune disorders, describing the mechanisms underlying both the therapeutic and secondary effects.
The innate and adaptive immune systems work as a complex interplay between different cell types, involving cytokines and chemokines mediating extracellular and paracrine effects. At the intracellular level, the inflammatory cascade is mediated by multifaceted processes that have been better described in the last 10 years. Immunosuppressive agents available in clinical practice act at different points of those cascades at the intracellular or extracellular level. Those drugs can mediate their effects on one or more cell types finally limiting inflammation and immune responses to antigens. Every immunosuppressive agent is characterized by intrinsic toxicity and side effects that may be due to the same therapeutic pathways or to off-target secondary effect of each molecule. We will here review the mechanisms of action of the most widely used immunosuppressive agents in the field of solid organ transplantation and autoimmune disorders, describing the mechanisms underlying both the therapeutic and secondary effects.The innate and adaptive immune systems work as a complex interplay between different cell types, involving cytokines and chemokines mediating extracellular and paracrine effects. At the intracellular level, the inflammatory cascade is mediated by multifaceted processes that have been better described in the last 10 years. Immunosuppressive agents available in clinical practice act at different points of those cascades at the intracellular or extracellular level. Those drugs can mediate their effects on one or more cell types finally limiting inflammation and immune responses to antigens. Every immunosuppressive agent is characterized by intrinsic toxicity and side effects that may be due to the same therapeutic pathways or to off-target secondary effect of each molecule. We will here review the mechanisms of action of the most widely used immunosuppressive agents in the field of solid organ transplantation and autoimmune disorders, describing the mechanisms underlying both the therapeutic and secondary effects.
ArticleNumber 101757
Author Bestard, Oriol
Meneghini, Maria
Grinyo, Josep Maria
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  orcidid: 0000-0001-7307-923X
  surname: Meneghini
  fullname: Meneghini, Maria
  email: mmeneghini@vhebron.net
  organization: Nephrology and Kidney Transplantation Unit. Vall D’Hebron University Hospital, Barcelona. Spain
– sequence: 2
  givenname: Oriol
  surname: Bestard
  fullname: Bestard, Oriol
  email: obestard@vhebron.net
  organization: Nephrology and Kidney Transplantation Unit. Vall D’Hebron University Hospital, Barcelona. Spain
– sequence: 3
  givenname: Josep Maria
  surname: Grinyo
  fullname: Grinyo, Josep Maria
  email: jgrinyo@ub.edu
  organization: University of Barcelona. Department of Clinical Sciences. Barcelona. Spain
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Allotransplantation
Immunosuppression
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Snippet The innate and adaptive immune systems work as a complex interplay between different cell types, involving cytokines and chemokines mediating extracellular and...
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SubjectTerms Acids
Allotransplantation
Autoimmune diseases
Autoimmunity
Binding sites
Bioavailability
Cell cycle
Clinical medicine
Cytokines
Dihydrofolate reductase
Drug dosages
Enzymes
Gene expression
Immunosuppression
Immunosuppressive agents
Kinases
Metabolism
Metabolites
Pharmacokinetics
Proteins
Steroids
Transcription factors
Transplants & implants
Title Immunosuppressive drugs modes of action
URI https://www.clinicalkey.com/#!/content/1-s2.0-S1521691821000378
https://dx.doi.org/10.1016/j.bpg.2021.101757
https://www.proquest.com/docview/2607316199
https://www.proquest.com/docview/2608131722
Volume 54-55
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