Inflammatory bowel disease (IBD) is a chronic inflammatory disorder and one of the most common inflammatory diseases of gastrointestinal (GI) tract in young adults. It is now equally prevalent in western countries as well as in Asian countries. Recently, there has been an increasing IBD burden in low- to middle-income countries as opposed to the earlier notion of this being a disease of the affluents. It occurs due to a variety of factors, namely, local immune alteration, disruption and inflammation of the mucosa, environmental factors, microbial commensals, and pathogen-induced genetic predisposition or genetic alteration in protective factors, etc. So far, an exact etiopathogenesis of IBD is yet to be completely elucidated. Several recent types of research have emphasized the role of altered innate and humoral immunity in its causation, many of them based on animal models of IBD. Due to the poor understanding of its etiopathogenesis, IBD is still a challenge for the treating clinicians leading to persistent and recurrent disease in many cases. Immune dysregulation in the GI tract incited by various pathogenic stimuli has gained great attention from researchers in the field of IBD. This review focuses on highlighting the role of various T cell subsets, their interplay, and associated cytokines involved in the pathogenesis of IBD along with a short description of genetic as well as other immunological factors. A better understanding of the pathogenic factors and subsequent randomized controlled trials targeting these factors is prudent for better therapeutic approaches for IBD.