We used IHC to identify and localize T cells and myeloid cells in PDA tumors, and performed flow cytometry on single cell suspensions of both tumor and peripheral blood on a subset of patients. Since immune checkpoint blockade has shown promise in the treatment of other malignancies, we examined whether the inhibitory receptor programmed death-1 was upregulated on T cells locally or systemically, and found that, in contrast to T cells in the peripheral blood, the majority of T cells in the PDA tumor microenvironment express PD-1. We also demonstrated that multimodal neoadjuvant therapy reduces the infiltration of PDA tumors by immunosuppressive cell types associated with reduced survival. We found that, while T cells and myeloid cells were rare in normal, non-neoplastic pancreatic parenchyma, both cell types were present both within the stroma and adjacent to carcinoma cells throughout PDA tumors. Since tumor differentiation in PDA has been shown to impact survival, we categorized tumors based upon standard histological criteria into well- to moderately differentiated or poorly differentiated. We determined the average numbers of CD3 + and CD11b + cells in regions containing carcinoma cells and found that T cells were significantly more prevalent than myeloid cells in both well-mod differentiated and poorly differentiated tumors. There were significantly more myeloid cells in poorly differentiated tumors, as well as a trend towards an increase in T cell infiltrate based upon tumor differentiation status. Importantly, we discovered a strong positive correlation between the density of T cell and myeloid cell infiltration in our specimens. We stained a subset of the specimens for GM-CSF to determine if there was a relationship between its expression in human PDA and the character of the immune infiltrate. Normal pancreas tissue showed minimal GM-CSF expression, while PDA tumors had a range of expression from low to high. There was no association between intratumoral GMCSF expression and the density of either the T cell or myeloid cell infiltrate, nor was a correlation observed between the intensity of GM-CSF staining and the differentiation status of tumor. Furthermore, we often observed CD3 positive cells overlying cancer glands in tumors with strong GM-CSF expression, demonstrating that tumor-derived GMCSF production does not directly or indirectly preclude T cell homing and infiltration in human PDA. The immune system is known to be intimately involved in the development, progression or control of multiple cancers, including PDA. Prior studies identified T cells infiltrating human PDA and demonstrated a positive relationship between the density of the T cell infiltrate and survival. In the present study, we used IHC and flow cytometry to characterize the immune infiltrate in PDA from both a qualitative and quantitative standpoint.