TLR7/9 antagonists as therapeutics for immune-mediated inflammatory disorders.
Identifieur interne : 001A54 ( Main/Exploration ); précédent : 001A53; suivant : 001A55TLR7/9 antagonists as therapeutics for immune-mediated inflammatory disorders.
Auteurs : Siquan Sun [États-Unis] ; Navin L. Rao ; Jennifer Venable ; Robin Thurmond ; Lars KarlssonSource :
- Inflammation & allergy drug targets [ 1871-5281 ] ; 2007.
Descripteurs français
- KwdFr :
- Adjuvants immunologiques (), Adjuvants immunologiques (pharmacologie), Adjuvants immunologiques (usage thérapeutique), Animaux, Humains, Inflammation (immunologie), Inflammation (physiopathologie), Inflammation (traitement médicamenteux), Maladies auto-immunes (physiopathologie), Maladies auto-immunes (traitement médicamenteux), Modèles immunologiques, Récepteur de type Toll-7 (antagonistes et inhibiteurs), Récepteur de type Toll-7 (physiologie), Récepteur-9 de type Toll-like (antagonistes et inhibiteurs), Récepteur-9 de type Toll-like (physiologie), Structure moléculaire.
- MESH :
- antagonistes et inhibiteurs : Récepteur de type Toll-7, Récepteur-9 de type Toll-like.
- immunologie : Inflammation.
- pharmacologie : Adjuvants immunologiques.
- physiologie : Récepteur de type Toll-7, Récepteur-9 de type Toll-like.
- physiopathologie : Inflammation, Maladies auto-immunes.
- traitement médicamenteux : Inflammation, Maladies auto-immunes.
- usage thérapeutique : Adjuvants immunologiques.
- Adjuvants immunologiques, Animaux, Humains, Modèles immunologiques, Structure moléculaire.
English descriptors
- KwdEn :
- Adjuvants, Immunologic (chemistry), Adjuvants, Immunologic (pharmacology), Adjuvants, Immunologic (therapeutic use), Animals, Autoimmune Diseases (drug therapy), Autoimmune Diseases (physiopathology), Humans, Inflammation (drug therapy), Inflammation (immunology), Inflammation (physiopathology), Models, Immunological, Molecular Structure, Toll-Like Receptor 7 (antagonists & inhibitors), Toll-Like Receptor 7 (physiology), Toll-Like Receptor 9 (antagonists & inhibitors), Toll-Like Receptor 9 (physiology).
- MESH :
- chemical , antagonists & inhibitors : Toll-Like Receptor 7, Toll-Like Receptor 9.
- chemical , chemistry : Adjuvants, Immunologic.
- chemical , pharmacology : Adjuvants, Immunologic.
- chemical , physiology : Toll-Like Receptor 7, Toll-Like Receptor 9.
- chemical , therapeutic use : Adjuvants, Immunologic.
- drug therapy : Autoimmune Diseases, Inflammation.
- immunology : Inflammation.
- physiopathology : Autoimmune Diseases, Inflammation.
- Animals, Humans, Models, Immunological, Molecular Structure.
Abstract
There is an increasing interest in ligands of nucleic acid-sensing Toll-like receptors (TLR), especially TLR7 and TLR9, for pharmacological intervention in various diseases. The TLR7 agonist imiquimod is currently used as a topical treatment for genital warts caused by human papillomavirus (HPV), actinic keratosis (AK) and superficial basal cell carcinoma. Oligodeoxynucleotides (ODN) TLR9 agonists are currently in clinical trials for use in lung cancer, as anti-viral therapy, as adjuvants and as immune modulators in asthma and allergies. TLR7/9 antagonists, such as the anti-malaria drugs chloroquine, hydroxychloroquine and quinacrine, have been used since the 1950s to treat immune-mediated inflammatory disorders (IMID) such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and Sjögren's syndrome. However, the use of these anti-malarials in IMID is limited due to the side effects or suboptimal efficacy. Pre-clinical animal models as well as genetic linkage studies have indicated that TLR7/9 play a pivotal role in the aforementioned as well as other IMID such as multiple sclerosis (MS), inflammatory bowl disease (IBD)/colitis and psoriasis. Recent evidence has suggested that selective, specific antagonists for TLR7 and/or 9 might be more beneficial in certain diseases, such as SLE. Thus, the use of suppressive ODN or novel small molecule TLR7/9 inhibitors with a larger safety window and differentiated selectivity may potentially have significant clinical utility in these IMID. Herein, we review efforts to develop novel TLR7/9 antagonists and the rationale for the use of such therapeutics in a variety of IMID.
DOI: 10.2174/187152807783334300
PubMed: 18220957
Affiliations:
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Le document en format XML
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Rao</name></author><author><name sortKey="Venable, Jennifer" sort="Venable, Jennifer" uniqKey="Venable J" first="Jennifer" last="Venable">Jennifer Venable</name></author><author><name sortKey="Thurmond, Robin" sort="Thurmond, Robin" uniqKey="Thurmond R" first="Robin" last="Thurmond">Robin Thurmond</name></author><author><name sortKey="Karlsson, Lars" sort="Karlsson, Lars" uniqKey="Karlsson L" first="Lars" last="Karlsson">Lars Karlsson</name></author></analytic><series><title level="j">Inflammation & allergy drug targets</title><idno type="ISSN">1871-5281</idno><imprint><date when="2007" type="published">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adjuvants, Immunologic (chemistry)</term><term>Adjuvants, Immunologic (pharmacology)</term><term>Adjuvants, Immunologic (therapeutic use)</term><term>Animals</term><term>Autoimmune Diseases (drug therapy)</term><term>Autoimmune Diseases (physiopathology)</term><term>Humans</term><term>Inflammation (drug therapy)</term><term>Inflammation (immunology)</term><term>Inflammation (physiopathology)</term><term>Models, Immunological</term><term>Molecular Structure</term><term>Toll-Like Receptor 7 (antagonists & inhibitors)</term><term>Toll-Like Receptor 7 (physiology)</term><term>Toll-Like Receptor 9 (antagonists & inhibitors)</term><term>Toll-Like Receptor 9 (physiology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adjuvants immunologiques ()</term><term>Adjuvants immunologiques (pharmacologie)</term><term>Adjuvants immunologiques (usage thérapeutique)</term><term>Animaux</term><term>Humains</term><term>Inflammation (immunologie)</term><term>Inflammation (physiopathologie)</term><term>Inflammation (traitement médicamenteux)</term><term>Maladies auto-immunes (physiopathologie)</term><term>Maladies auto-immunes (traitement médicamenteux)</term><term>Modèles immunologiques</term><term>Récepteur de type Toll-7 (antagonistes et inhibiteurs)</term><term>Récepteur de type Toll-7 (physiologie)</term><term>Récepteur-9 de type Toll-like (antagonistes et inhibiteurs)</term><term>Récepteur-9 de type Toll-like (physiologie)</term><term>Structure moléculaire</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Toll-Like Receptor 7</term><term>Toll-Like Receptor 9</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Adjuvants, Immunologic</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Adjuvants, Immunologic</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Toll-Like Receptor 7</term><term>Toll-Like Receptor 9</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Adjuvants, Immunologic</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Récepteur de type Toll-7</term><term>Récepteur-9 de type Toll-like</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Autoimmune Diseases</term><term>Inflammation</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Inflammation</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Inflammation</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Adjuvants immunologiques</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Récepteur de type Toll-7</term><term>Récepteur-9 de type Toll-like</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Inflammation</term><term>Maladies auto-immunes</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Autoimmune Diseases</term><term>Inflammation</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Inflammation</term><term>Maladies auto-immunes</term></keywords><keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Adjuvants immunologiques</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term><term>Models, Immunological</term><term>Molecular Structure</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adjuvants immunologiques</term><term>Animaux</term><term>Humains</term><term>Modèles immunologiques</term><term>Structure moléculaire</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">There is an increasing interest in ligands of nucleic acid-sensing Toll-like receptors (TLR), especially TLR7 and TLR9, for pharmacological intervention in various diseases. The TLR7 agonist imiquimod is currently used as a topical treatment for genital warts caused by human papillomavirus (HPV), actinic keratosis (AK) and superficial basal cell carcinoma. Oligodeoxynucleotides (ODN) TLR9 agonists are currently in clinical trials for use in lung cancer, as anti-viral therapy, as adjuvants and as immune modulators in asthma and allergies. TLR7/9 antagonists, such as the anti-malaria drugs chloroquine, hydroxychloroquine and quinacrine, have been used since the 1950s to treat immune-mediated inflammatory disorders (IMID) such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and Sjögren's syndrome. However, the use of these anti-malarials in IMID is limited due to the side effects or suboptimal efficacy. Pre-clinical animal models as well as genetic linkage studies have indicated that TLR7/9 play a pivotal role in the aforementioned as well as other IMID such as multiple sclerosis (MS), inflammatory bowl disease (IBD)/colitis and psoriasis. Recent evidence has suggested that selective, specific antagonists for TLR7 and/or 9 might be more beneficial in certain diseases, such as SLE. Thus, the use of suppressive ODN or novel small molecule TLR7/9 inhibitors with a larger safety window and differentiated selectivity may potentially have significant clinical utility in these IMID. Herein, we review efforts to develop novel TLR7/9 antagonists and the rationale for the use of such therapeutics in a variety of IMID.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Californie</li></region></list><tree><noCountry><name sortKey="Karlsson, Lars" sort="Karlsson, Lars" uniqKey="Karlsson L" first="Lars" last="Karlsson">Lars Karlsson</name><name sortKey="Rao, Navin L" sort="Rao, Navin L" uniqKey="Rao N" first="Navin L" last="Rao">Navin L. Rao</name><name sortKey="Thurmond, Robin" sort="Thurmond, Robin" uniqKey="Thurmond R" first="Robin" last="Thurmond">Robin Thurmond</name><name sortKey="Venable, Jennifer" sort="Venable, Jennifer" uniqKey="Venable J" first="Jennifer" last="Venable">Jennifer Venable</name></noCountry><country name="États-Unis"><region name="Californie"><name sortKey="Sun, Siquan" sort="Sun, Siquan" uniqKey="Sun S" first="Siquan" last="Sun">Siquan Sun</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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