Background: Biological therapies using anti-tumor necrosis factor (TNF)-α agents have an important impact in the treatment of inflammatory bowel disease, rheumatoid arthritis, psoriasis, and other inflammatory conditions. However, a significant number of patients lose their response to these medications over time. Clinical trials have demonstrated that antibodies against anti-TNF agents may impact treatment response and increase the risk of infusion reactions. Of concern is also the possibility of developing adverse events induced by anti-TNF agents. The purpose of the present systematic review is to describe the current knowledge on the risk of infections associated with anti-TNF agents antagonists, as well as integrin antagonists. We also intend to describe case reports of these adverse events in inflammatory bowel disease patients. Methods: Currently approved anti-TNF biologicals in IBD include the monoclonal antibodies infliximab, adalimumab, certolizumab pegol and golimumab. Integrin antagonists include natalizumab, etrolizumab and vedolizumab. Results: The most frequently-reported adverse events of these biologicals were infections, and these are described in detail in this study. Discussion: Most adverse events are due to the failure of host immunological control, which involves de novo infection, or reactivation of latent bacterial or viral infection, often with a different expression of disease. Conclusion: Risk assessment in individuals undergoing treatment with biologicals represents a step towards achieving treatment personalization to identify those patients that will safely benefit from this therapeutic approach. Patients and physicians must be alert for anti-TNF agents and anti-integrin medication as potential causes of drug-induced infections and monitor the therapies. Personalizing therapeutic vigilance promises to optimize benefits while minimizing infections.This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.