In the present work, we introduce a rapid Sulfamethazine cavitation procedure to isolate T. cruzi amastigotes from Vero cells. In this protocol, cavitation by nitrogen decompression is followed by a few centrifugation steps, allowing the rapid purification of viable intracellular amastigotes that are competent for endocytosis. Flow cytometry, fluorescence microscopy and western blotting analyses demonstrated that the T. cruzi amastigotes isolated using this new methodology were capable of internalizing transferrin and albumin from the extracellular milieu, and that these molecules were directed efficiently to LROs. Importantly, we detected co-localization of ingested transferrin and albumin with cruzipain, in LROs. Our data also suggest that the LROs of T. cruzi intracellular amastigotes correspond to reservosomes. T2D is a metabolic disorder characterized by defects in glucose uptake in response to insulin. Although T2D is not considered as autoimmune disease traditionally, its state is linked with altered immune response including low graded inflammation had been revealed. In addition, several reports confirmed that patients with RA had characteristics placing the mat high risk for T2D. However, the correlation between RA and T2D cannot been ruled out, and whether the association is related with immune response has not yet been illuminated, especially in the lack of comprehensive study to look at the molecular association and commonly shared mechanisms between these two KRP-203 disorders. The disturbance of signaling pathways on inflammation and immune response was considered as one of important reasons for both RA and T2D respectively. Evidences implicated that the pro-inflammatory cytokines TNF-�� and IL-6, which were key mediators of inflammation in RA, were overproduced in visceral adipose tissue and impaired insulin receptor signaling to cause insulin resistance in T2D. Other inflammatory cytokines, such as elevated levels of IL-2in both serum and synovial tissues were appeared to be associated with both RA and T2D, and correlated with insulin sensitivity in patients with RA. However, the complex interactions among cytokines in RA and T2D were yet to be fully elucidated.