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The function of nesfatin-1, corresponding to the nucleobindin2 (NUCB2) precursor, was first identified in the hypothalamic nuclei, and was reported to be potently anorexigenic (Oh-I et al. 2006). More recently it has been shown that expression of Nesfatin-1 is not restricted locally to the hypothalamus but is widely expressed in many peripheral tissues, including adipose tissue, and associated with a range of physiological effects. For example, when Nesfatin-1 is genetically knocked out ( Nucb2-/-) in mice fed a high fat diet there is a resultant increase in the gene expression of pro-inflammatory mediators and cytokines, including Tlr4, in the subcutaneous white adipose tissue compared to WT animals also fed a high fat diet. These data support that Nesfatin-1 has anti-inflammatory properties, but the mechanistic actions of this peptide in this setting have yet to be fully described (Gharane et al. 2022). To begin to evaluate the interactions of Nesfantin-1 and immune cells more in depth we began with B lymphocytes where Nubc2, the Nesfatin-1 precursor, was originally identified (Miura et al. 1993). Using an immortalized B lymphocyte cell line, Raji, and primary cells from human donors we determined the ability of Nesfatin-1 to bind to the cell surface and affect B lymphocyte proliferation. Furthermore, we determined if treatment with Nesfatin-1 is sufficient to protect against toll like receptor-4 (TLR4) and B cell receptor (BCR) induced cytokine and antibody release from B lymphocytes. This work is the beginning characterization of a novel interaction between Nesfatin-1 and B cells. Given the anti-inflammatory activity of Nesfatin-1 and its potential direct effects on immune cells, there is a broader impact for this work in protection during chronic inflammation caused by obesity and metabolic disorders. Saint Louis University This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.