Insulin-like Growth Factor 1 (IGF-1) is a hormone that plays an important role in growth, development, and metabolism. Little is known about its ability to regulate immune function. This study sought to address whether IGF-1 plays an inflammatory or anti-inflammatory role during an immune response. Our findings suggest that an upregulation of its primary receptor, IGF-1R, is indicative of an inflammation. Blood was drawn from 16 dogs and analyzed via flow cytometry for proteins consistent with an inflammatory phenotype. Samples from 10 dogs were stained with anti-CD11b, anti-CD14, and anti-IGF-1R. Samples from the remaining 6 dogs were stained for anti-CD14, anti-CD4, and IGF-1R directly bound to APC in 6 dogs. We suspect that using IGF-1 rather than its antibody will demonstrate a more physiological response, i.e. one more akin to what would take place in the dog. We found that expression of CD14, a co-receptor for TLR’s that  is widely used as a marker for monocytes, is upregulated as IGF-1R levels increase, suggesting that the number of canine monocytes increases as IGF-1R levels do. We then asked if a particular subpopulation of monocytes upregulated IGF-1R at higher rates. Using a gating scheme designed by Sampath Kumar and Alex Crane, we distinguished what we believe to be inflammatory  classical monocytes from non-classical monocytes, which are thought to be imbued with suppressive function, using anti-CD4. Our IGF-1R stains suggest that a population of CD4- monocytes, i.e. classical monocytes, upregulate IGF-1R. This is consistent with our hypothesis that IGF-1R is associated with inflammation. Lastly, this study evaluated CD11b expression. CD11b is an integrin protein and myeloid marker that is correlated with activation status of an immune cell and can also be used as an inflammatory marker. We found that CD11b, like CD14, increases as IGF-1R expression increases, albeit at a smaller rate.