Abstract
Crohn’s Disease (CD) results from inappropriate response toward commensal flora. Earlier studies described CD as a Th1 mediated disease. Current models view both phenotypes as a continuum of various permutations between Th1, Th2 and Th17 pathways compounded by a range of Treg disfunctions. In the present paper, we develop a mathematical model, by a system of differential equations, which describe the dynamic relations among these T cells and their cytokines. The model identities four groups of CD patients according to up/down regulation of Th1 and Th2. The model simulations show that immunosuppression by TNF-α blockage benefits the group with Th1High/Th2Low while, by contrast, the group with Th1Low/Th2High will benefit from immune activation.
Highlights
Inflammatory Bowel Diseases (IBD), Crohn’s Disease (CD) and Ulcerative Colitis (UC) result from an inappropriate immune response toward commensal flora [1]
Patients with inflammatory bowel diseases have elevated levels of circulating and gut mucosal cytokines [1]. Downstream signaling from these inflammatory mediators, through Janus kinase (JAK) and signal transducers and activators of transcription (STAT) proteins, activate transcription factors T-bet, GATA3, Foxp3 and RORγt [3]
Earlier animal and human studies described CD as a T helper 1 (Th1) mediated [5]. Current models view both phenotypes as a continuum of various permutations between the Th1, Th2, and Th17 pathways compounded by a range of Th17 and regulatory (Treg) dysfunctions [4]
Summary
Inflammatory Bowel Diseases (IBD), Crohn’s Disease (CD) and Ulcerative Colitis (UC) result from an inappropriate immune response toward commensal flora [1]. Patients with inflammatory bowel diseases have elevated levels of circulating and gut mucosal cytokines [1]. Downstream signaling from these inflammatory mediators, through Janus kinase (JAK) and signal transducers and activators of transcription (STAT) proteins, activate transcription factors T-bet, GATA3, Foxp and RORγt [3]. Earlier animal and human studies described CD as a Th1 mediated [5]. Current models view both phenotypes as a continuum of various permutations between the Th1, Th2, and Th17 pathways compounded by a range of Treg dysfunctions [4]
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