Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab (Humira), and certolizumab (Cimzia), are approved for treating inflammatory bowel disease (IBD), including Crohn's disease.

Infliximab, adalimumab, and golimumab belong to the IgG1 subclass, while certolizumab is a recombinant antibody with a Fab fragment conjugated to PEG. These antibodies work by binding to and neutralizing both soluble and membrane-bound TNF, preventing its binding to receptors and mitigating the inflammatory response in Crohn's disease. They lead to symptomatic improvement and remission. Infliximab is administered intravenously, while adalimumab, golimumab, and certolizumab are given subcutaneously. Adverse effects of these anti-TNF therapies include infusion reactions, respiratory infections, reactivation of latent tuberculosis, and the development of antibodies against the drugs.