Emerging studies indicate that the immune system can regulate adipose tissue. Type II immune cells, such as group II innate lymphocytes (ILC2s) and eosinophils, induce adipose beiging, promoting thermogenic expenditure and decreased adipose mass. T regulatory cells (Tregs) suppress the inflammation associated with increased adiposity and thereby maintain insulin sensitivity. Exploitation of signals that activate these cells types could lead to novel therapeutics for metabolic syndrome. In this work, we show that Thymic Stromal Lymphopoietin (TSLP), a type II cytokine that expands both type II immune cells and Tregs, induces selective white adipose loss. TSLP also protected mice against obesity, type II diabetes, and non-alcoholic steatohepatitis (NASH). Surprisingly, the adipose loss was not caused by alterations in food intake, absorption, or energy expenditure. Rather, it was caused by the excessive loss of lipids through the skin as sebum. Furthermore, the adipose loss was mediated by T cells, but not Tregs, ILC2s, eosinophils, basophils, or monocytes. At homeostasis, TSLP and T cells regulated sebum release and sebum-associated anti-microbial peptide expression. In human skin, TSLP and sebum-related gene expression were positively correlated. Together, our study provides novel proof-of-concept that adipose loss can be achieved by sebum hypersecretion and reveals a previously unknown role of adaptive immunity in promoting skin barrier function through sebum secretion.