Is it wise to target the late costimulatory molecule OX40 as a therapeutic target?Citation formats

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Is it wise to target the late costimulatory molecule OX40 as a therapeutic target? / Cavanagh, Mary Miranda; Hussell, Tracy.

In: Archivum Immunologiae et Therapiae Experimentalis, Vol. 56, No. 5, 10.2008, p. 291-297.

Research output: Contribution to journalArticle

Harvard

Cavanagh, MM & Hussell, T 2008, 'Is it wise to target the late costimulatory molecule OX40 as a therapeutic target?', Archivum Immunologiae et Therapiae Experimentalis, vol. 56, no. 5, pp. 291-297. https://doi.org/10.1007/s00005-008-0032-3

APA

Cavanagh, M. M., & Hussell, T. (2008). Is it wise to target the late costimulatory molecule OX40 as a therapeutic target? Archivum Immunologiae et Therapiae Experimentalis, 56(5), 291-297. https://doi.org/10.1007/s00005-008-0032-3

Vancouver

Author

Cavanagh, Mary Miranda ; Hussell, Tracy. / Is it wise to target the late costimulatory molecule OX40 as a therapeutic target?. In: Archivum Immunologiae et Therapiae Experimentalis. 2008 ; Vol. 56, No. 5. pp. 291-297.

Bibtex

@article{12496d8466ef40e69fa25a930fa49db6,
title = "Is it wise to target the late costimulatory molecule OX40 as a therapeutic target?",
abstract = "The immune response triggered following pathogen recognition, though required to clear the infection, can be detrimental if it is produced in excess or fails to resolve promptly. Excessive inflammation contributes to infectious and noninfectious pathologies in the gut (such as inflammatory bowel disease), lung (such as bronchiolitis), and in a variety of autoimmune conditions. T cells contribute significantly to pathology during inflammation. Global anti-inflammatory strategies can alleviate the consequences of exuberant inflammation by suppressing T cell activity, but may leave the patient vulnerable to opportunistic infection. More specific therapies aim to suppress only those T cells involved in the disease process, and one such approach is to target late costimulatory molecules. These are not expressed on na{\"i}ve or resting memory cells. Rather, they have a specific window of expression and their ligation results in the production of abundant inflammatory cytokines. By targeting these molecules, it is hoped that inflammation will reduce, but that therapies will be specific enough to avoid, global immune suppression. This review focuses on the late costimulatory molecule OX40, compare it with other T cell costimulators, and highlight why it is a more suitable target for immune intervention than other immune suppressive strategies. {\circledC} 2008 Birkhaueser.",
keywords = "Autoimmunity, Costimulatory molecules, Immunopathology, Infection, OX40",
author = "Cavanagh, {Mary Miranda} and Tracy Hussell",
year = "2008",
month = "10",
doi = "10.1007/s00005-008-0032-3",
language = "English",
volume = "56",
pages = "291--297",
journal = "Archivum Immunologiae et Therapiae Experimentalis",
issn = "1661-4917",
publisher = "Birkh{\"a}user Verlag Ag",
number = "5",

}

RIS

TY - JOUR

T1 - Is it wise to target the late costimulatory molecule OX40 as a therapeutic target?

AU - Cavanagh, Mary Miranda

AU - Hussell, Tracy

PY - 2008/10

Y1 - 2008/10

N2 - The immune response triggered following pathogen recognition, though required to clear the infection, can be detrimental if it is produced in excess or fails to resolve promptly. Excessive inflammation contributes to infectious and noninfectious pathologies in the gut (such as inflammatory bowel disease), lung (such as bronchiolitis), and in a variety of autoimmune conditions. T cells contribute significantly to pathology during inflammation. Global anti-inflammatory strategies can alleviate the consequences of exuberant inflammation by suppressing T cell activity, but may leave the patient vulnerable to opportunistic infection. More specific therapies aim to suppress only those T cells involved in the disease process, and one such approach is to target late costimulatory molecules. These are not expressed on naïve or resting memory cells. Rather, they have a specific window of expression and their ligation results in the production of abundant inflammatory cytokines. By targeting these molecules, it is hoped that inflammation will reduce, but that therapies will be specific enough to avoid, global immune suppression. This review focuses on the late costimulatory molecule OX40, compare it with other T cell costimulators, and highlight why it is a more suitable target for immune intervention than other immune suppressive strategies. © 2008 Birkhaueser.

AB - The immune response triggered following pathogen recognition, though required to clear the infection, can be detrimental if it is produced in excess or fails to resolve promptly. Excessive inflammation contributes to infectious and noninfectious pathologies in the gut (such as inflammatory bowel disease), lung (such as bronchiolitis), and in a variety of autoimmune conditions. T cells contribute significantly to pathology during inflammation. Global anti-inflammatory strategies can alleviate the consequences of exuberant inflammation by suppressing T cell activity, but may leave the patient vulnerable to opportunistic infection. More specific therapies aim to suppress only those T cells involved in the disease process, and one such approach is to target late costimulatory molecules. These are not expressed on naïve or resting memory cells. Rather, they have a specific window of expression and their ligation results in the production of abundant inflammatory cytokines. By targeting these molecules, it is hoped that inflammation will reduce, but that therapies will be specific enough to avoid, global immune suppression. This review focuses on the late costimulatory molecule OX40, compare it with other T cell costimulators, and highlight why it is a more suitable target for immune intervention than other immune suppressive strategies. © 2008 Birkhaueser.

KW - Autoimmunity

KW - Costimulatory molecules

KW - Immunopathology

KW - Infection

KW - OX40

U2 - 10.1007/s00005-008-0032-3

DO - 10.1007/s00005-008-0032-3

M3 - Article

VL - 56

SP - 291

EP - 297

JO - Archivum Immunologiae et Therapiae Experimentalis

JF - Archivum Immunologiae et Therapiae Experimentalis

SN - 1661-4917

IS - 5

ER -