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.

Abstract: The present invention relates to methods of prognosing responsiveness to anti-TNF? therapy by determining the presence or absence of risk factors in the individual. In one embodiment, the risk factors are genetic markers, serological markers and/or clinical phenotypes associated with non-responsiveness to treatment with anti-TNF? therapy in an individual diagnosed with IBD.

Abstract: Described herein are systems and methods for stratifying intestinal mononuclear phagocytes (MNP) expression profiles in subjects with an inflammatory bowel disease (IBD). Further provided herein are systems and methods for determining or characterizing a Crohn's Disease (CD) subtype status in a subject having CD, selecting a treatment for a subject, or treating a subject.

Abstract: Described herein are humanized anti-TL1A antibodies and pharmaceutical compositions for the treatment of inflammatory bowel disease (IBD), such as Crohn's Disease (CD) and ulcerative colitis (UC).

Abstract: Described herein are humanized anti-TL1A antibodies and pharmaceutical compositions for the treatment of diseases and/or conditions in the lung.

Abstract: This invention provides methods of diagnosis, predicting and diagnosing susceptibility to, predicting disease progression and treatment of inflammatory bowel disease (IBD), including Crohn's disease and/or subtypes of Crohn's disease (CD) and/or Ulcerative Colitis (UC). In one embodiment, a method of the invention is practiced by determining the presence or absence of the genetic variants NOD2, TLR8, TLR2, CARD8, CARD15 and/or JAK3 to diagnose, predict and diagnose susceptibility and predict disease progression in an individual. In another embodiment, a method of the invention is practiced by determining the presence or absence of anti-Cbir1, anti-OmpC, ASCA, anti-I2 and/or pANCA in an individual. In another embodiment, the invention further associates the presence or absence of the risk variants with the expression of anti-Cbir1, anti-OmpC, ASCA, anti-I2 and/or pANCA for the diagnosis, prediction of susceptibility, prediction of disease progression and/or treatment of IBD, including CD and/or UC.

Abstract: Described herein are humanized anti-TL1A antibodies and pharmaceutical compositions for the treatment of inflammatory bowel disease (IBD), such as Crohn's Disease (CD) and ulcerative colitis (UC).

Abstract: Described herein are humanized anti-TL1A antibodies and pharmaceutical compositions for the treatment of inflammatory bowel disease (IBD), such as Crohn's Disease (CD) and ulcerative colitis (UC).

Abstract: The present invention relates to methods of prognosing responsiveness to anti-TNF? therapy by determining the presence or absence of risk factors in the individual. In one embodiment, the risk factors are genetic markers, serological markers and/or clinical phenotypes associated with non-responsiveness to treatment with anti-TNF? therapy in an individual diagnosed with IBD.

Abstract: The aspects disclosed herein describe methods of identifying a subject that is non-responsive to anti-TNF therapy. The aspects disclosed herein further provide for a method of selecting a therapy for a subject with Inflammatory Bowel Disease (IBD), and treating the subject with the therapy.

Abstract: Described herein are humanized anti-TL1A antibodies and pharmaceutical compositions for the treatment of inflammatory bowel disease (IBD), such as Crohn's Disease (CD) and ulcerative colitis (UC).

Abstract: Described herein are methods and pharmaceutical compositions for the treatment of inflammatory bowel disease (IBD), Crohn's Disease (CD), ulcerative colitis (UC) and medically refractive-ulcerative colitis (MR-UC). In particular, disclosed are anti-TL1A antibodies useful for the treatment of IBD.

Abstract: Disclosed herein are methods, kits and compositions for treating an inflammatory disease or condition, or fibrosis in a subject that has been determined to have increased fold-change in Tumor necrosis factor (TNF)-like cytokine 1A (TL1A) expression based, at least partially, on a presence of a combination of genotypes detected in a sample obtained from the subject. In some embodiments, the combination of genotypes is significantly associated with the increased fold-change in TL1A, and in some cases, may also be predictive of severe forms of the inflammatory disease or condition. In some embodiments, the inflammatory disease or condition is an inflammatory bowel disease, such as Crohn's disease or ulcerative colitis.

Abstract: Described herein are methods, systems, compositions, and kits useful for identifying patients as having a high likelihood of recurrence of a disease or condition affecting the gastrointestinal tract following surgical treatment of the disease or condition. The present disclosure relates to methods and systems for identifying and stratifying patients, suitable for treatment with a modulator of RNASET2, as described herein.

Abstract: Described herein are methods and systems for identifying subpopulations of patients having Crohn's disease, including populations at risk of developing stricturing or other severe disease, and populations susceptible to success or failure with surgical intervention. Further provided are therapies useful for treating subpopulations of patients having Crohn's disease.

Abstract: Described herein are humanized anti-TL1A antibodies and pharmaceutical compositions for the treatment of inflammatory bowel disease (IBD), such as Crohn's Disease (CD) and ulcerative colitis (UC).

Abstract: The invention relates to methods of treating fibrosis and inflammatory bowel disease. In one embodiment, the present invention treats gut inflammation by administering a therapeutically effective dosage of TL1A inhibitors and/or DR3 inhibitors to an individual. In another embodiment, the present invention provides a method of reversing tissue fibrosis in an individual by inhibiting TL1A-DR3 signaling function.

Abstract: Described herein are methods and systems for identifying subpopulations of patients having Crohn's disease, including populations at risk of developing structuring or other severe disease, and populations susceptible to success or failure with surgical intervention. Further provided are therapies useful for treating subpopulations of patients having Crohn's disease.

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.

Abstract: Organs-on-chips are microfluidic devices for culturing living cells in micrometer sized chambers in order to model physiological functions of tissues and organs. Engineered patterning and continuous fluid flow in these devices has allowed culturing of intestinal cells bearing physiologically relevant features and sustained exposure to bacteria while maintaining cellular viability, thereby allowing study of inflammatory bowl diseases. However, existing intestinal cells do not possess all physiologically relevant subtypes, do not possess the repertoire of genetic variations, or allow for study of other important cellular actors such as immune cells. Use of iPSC-derived epithelium, including IBD patient-specific cells, allows for superior disease modeling by capturing the multi-faceted nature of the disease.