Adipose tissue in the obese state can lead to low-grade chronic inflammation while inducing or exacerbating obesity-related metabolic diseases and impairing overall health.T cells, which are essential immune cells similar to macrophages, are widely distributed in adipose tissue and perform their immunomodulatory function; they also cross-talk with other cells in the vascular stromal fraction. Based on a large number of studies, it has been found that N6 methyl adenine (m6A) is one of the most representative of epigenetic modifications, which affects the crosstalk between T cells, as well as other immune cells, in several ways and plays an important role in the development of adipose tissue inflammation and related metabolic diseases. In this review, we first provide an overview of the widespread presence of T cells in adipose tissue and summarize the key role of T cells in adipose tissue inflammation. Next, we explored the effects of m6A modifications on T cells in adipose tissue from the perspective of adipose tissue inflammation. Finally, we discuss the impact of m6a-regulated crosstalk between T cells and immune cells on the prospects for improving adipose tissue inflammation research, providing additional new ideas for the treatment of obesity. This review investigates adipose tissue inflammation occurring in obesity, which is closely associated with metabolic disorders such as type 2 diabetes and nonalcoholic fatty liver disease. T cells, as immune cells infiltrating adipose tissue, deeply participate in the inflammatory process, while m6A serves as a novel regulatory mechanism in various physiological processes. The review explores the role of m6A in T cells during adipose tissue inflammation and its regulation of interactions between T cells and immune cells like macrophages and dendritic cells within the stromal vascular fraction (SVF). By linking m6A regulation with T cells in obese adipose tissue, it aims to offer new perspectives for research and treatment of obesity-related metabolic diseases.