With over one-third of US adults considered obese and an even larger proportion of adults and children being classified as overweight, the prevention and management of obesity has never been more crucial. The burden associated with obesity and its related comorbidities (ORC), including type 2 diabetes (T2DM), cardiovascular disease (CVD), hypertension (HTN), and obstructive sleep apnea (OSA), is tremendous, both in terms of direct costs to the healthcare system and indirect costs associated with decreased productivity. Despite this burden, there are relatively few treatments available for obesity. Currently, bariatric surgery (BS) is the most effective treatment modality for obesity and ORC with laparoscopic Roux-en Y gastric bypass (LRYGB) and laparoscopic sleeve gastrectomy (LSG) being the two most commonly performed procedures. Numerous studies support the clinical superiority of BS over intensive medical weight loss, with many patients experiencing upwards of 60% excess body weight loss (EBWL) and complete remission of T2DM and HTN within two years of BS. For these reasons, along with the decreasing morbidity and mortality, the number of BS has exponentially increased during this time to meet the demand for this important, life-saving procedure. Contiguous with the rise of surgical weight loss, our understanding of the pathophysiology of obesity and adipose tissue physiology has significantly expanded. The Hsueh laboratory has been instrumental in delineating the interconnection between the adipocyte and adipose tissue inflammation in obesity. Pivotal studies in murine models demonstrated that visceral adipose tissue is significantly more inflamed following high fat diet and is characterized by reductions in immunosuppressive regulatory T cells (Tregs) and increased pro-inflammatory M1-like macrophages, T helper Type 1 cells (Th1s), and neutrophils as compared to chow fed controls. Furthermore, murine adipocytes become pro-inflammatory immune antigen-presenting cells at the expense of their metabolic function during high fat diet feeding. This process is driven primarily by the upregulation of major histocompatibility complex II (MHCII) which stimulates naive helper T cells to differentiate into pro-inflammatory helper T cells (Th1) and thus suppress the production of adipose tissue Tregs. Importantly, mice with an adipocyte-specific MHCII knockout on a pro-atherogenic background demonstrate significant improvements in insulin sensitivity, atherosclerotic plaque development, and fatty liver disease, further emphasizing the adipocyte’s importance as a pro-inflammatory immune cell. We found similar changes in the adipocyte-T cell landscape in obese humans and reported that visceral and subcutaneous adipose tissue depots were markedly more inflamed, with reduced Tregs and increased pro-inflammatory adipocytes and macrophages as compared to lean controls. As with mice, reduced adipose tissue Treg abundance was associated with increased insulin resistance and positively correlated with increasing body mass index. Within our bariatric patients, we further discovered that reduced preoperative visceral Treg abundance was associated with higher disease severity for ORC, including insulin-dependent diabetes, preoperative statin use and need for multiple anti-hypertensive agents at baseline. While LRYGB and LSG are well-tolerated operations with reportedly excellent outcomes in the short-term, weight regain, comorbidity recidivism, and micronutrient deficiencies are significant post-operative complications that require long-term follow up and management. Despite the comparative success of BS and our advances in understanding the pathophysiology of obesity, the relationship between adipose tissue inflammation and surgical weight loss and its impact on long-term post-surgical outcomes remains unexplored. We discovered that one year post-operatively over one-third of our LSG patients were within the bottom quartile of EBWL outcomes, corresponding to less than 40% EBWL, which rose to 52% by two years and 69% by 3 years. In fact, this metric is considered “weight loss failure” after BS (