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RESEARCH PRODUCT
RUNX3 and T-Bet in Immunopathogenesis of Ankylosing Spondylitis—Novel Targets for Therapy?
Matteo VecellioMatteo VecellioMatteo VecellioCarla J. CohenCarla J. CohenCarla J. CohenAmity R. RobertsPaul B. WordsworthPaul B. WordsworthPaul B. WordsworthTony J. KennaTony J. Kennasubject
lcsh:Immunologic diseases. Allergy0301 basic medicineTBX21Mini ReviewImmunologyBiologyCD8-Positive T-Lymphocytesmedicine.disease_causeAminopeptidasesInterleukin-23Polymorphism Single NucleotideAutoimmunity03 medical and health sciences0302 clinical medicineankylosing spondylitisInterleukin 23medicineImmunology and AllergyHumansImmunologic FactorsSpondylitis AnkylosingMolecular Targeted TherapyInterleukin-7 receptorTranscription factorHLA-B27 AntigenAnkylosing spondylitistherapyAntigen processingautoimmunityReceptors Interleukinmedicine.disease3. Good healthKiller Cells Natural030104 developmental biologyCore Binding Factor Alpha 3 SubunitGene Expression RegulationinflammationImmunologylcsh:RC581-607T-Box Domain ProteinsFunctional genomicsfunctional genomics030215 immunologydescription
Susceptibility to ankylosing spondylitis (AS) is polygenic with more than 100 genes identified to date. These include HLA-B27 and the aminopeptidases (ERAP1, ERAP2, and LNPEPS), which are involved in antigen processing and presentation to T-cells, and several genes (IL23R, IL6R, STAT3, JAK2, IL1R1/2, IL12B, and IL7R) involved in IL23 driven pathways of inflammation. AS is also strongly associated with polymorphisms in two transcription factors, RUNX3 and T-bet (encoded by TBX21), which are important in T-cell development and function. The influence of these genes on the pathogenesis of AS and their potential for identifying drug targets is discussed here.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2019-01-10 | Frontiers in Immunology |