Signature of TL1A (TNFSF15) signaling pathway
AssigneeCedars-Sinai Medical Center
InventorsKathrin S. Michelsen, Stephan R. Targan
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Abstract
The present invention relates to the finding that TL1A enhances differentiation of TH17 cells, and enhance IL17 secretion from TH17 cells. In one embodiment, the present invention provides a method of treating an inflammatory disease comprising determining the presence of a TL1A signaling profile, and treating the disease by administering a composition comprising a therapeutically effective dosage of one or more inhibitors of TL1A or TH17 cell differentiation. In another embodiment, the disease is characterized by TH17 differentiation.
Claims15
A method of treating an inflammatory disease in a subject, the method comprising:
- determining an elevated level of interleukin 22 (IL-22) in a biological sample obtained from the subject as compared to a control level of IL-22 in an individual that does not have the inflammatory disease;
- determining a presence of one or more genetic risk variants at TNFSF15 in the biological sample and/or determining an elevated level of a transcription factor in the biological sample relative to a control level of the transcription factor in the individual that does not have the inflammatory disease, wherein the transcription factor comprises RAR Related Orphan Receptor A (RORA), T-Box Transcription Factor 21 (T-bet), or a combination thereof;
- and
- administering to the subject an anti-tumor necrosis factor-like cytokine 1A (TL1A) antibody or antigen-binding fragment thereof.
Dependencies are inferred from the claim text.