Meir Djaldetti

Human adenosine receptor bearing lymphocytes: Enumeration, characterization, and distribution in peripheral blood lymphocytes

Abstract Ox red blood cells (Ox-RBC) which were coated with adenosine covalently linked to human serum albumin (HSA) formed rosettes with a minor population of human peripheral blood lymphocytes (PBL) 2 . An average of 10.7% of total circulating PBL were capable of forming adenosine-specific rosettes and the majority of these cells (84%) were found in the spontaneous sheep E-rosetting cell population. The lymphocyte receptor was specific for the adenosine moiety in that HSA-coated Ox-RBC alone, or guanosine-HSA-coated Ox-RBC bound less that 2% of total PBL. In addition, the binding of the adenosine-HSA-coated Ox-RBC to the lymphocytes could be competitively inhibited by adenosine-HSA, adenosine, and low levels of theophylline but not by inosine or guanosine. The majority of the lymphocytes forming the adenosine-HSA rosettes appeared as small resting lymphocytes when examined by electron microscopy.

About the Role of Insulin in the Interaction Between Human Immune and Colon Cancer Cells

Background: Insulin has been one of the immense contributions to human health. Besides its role in treatment of diabetes, insulin affects inflammatory cytokine production, chronic inflammation and cancer development. We have examined the effect of insulin on cytokine production by human peripheral blood mononuclear cells (PBMC) and its role in the balance between immune and human colon cancer cells. n nMethods: Human LPS stimulated and non-stimulated PBMC, HT-29 and RKO cancer cell lines were separately incubated with insulin at various concentrations and the production of TNFα, IL-1β, IL-6, IFNγ, IL-1ra and IL-10 was examined. In addition, the effect of insulin on the secretion of these cytokines by PBMC co-incubated with carcinoma cells was evaluated.xa0 n nResults: Insulin added to non-stimulated PBMC caused a decreasaed secretion of the pro-inflammatory TNFα. Stimulation of PBMC with either LPS or PMA resulted in decreased production of IL-1β, TNFα and IFNγ and an increased generation of IL-6. The production of the anti-inflammatory cytokine IL-10 was elevated by both stimulated and unstimulated PBMC. Insulin added to PBMC inhibited the secretion of IFNγ stimulated with both HT-29 and RKO cells and reduced TNFα production induced by RKO cells. n nConclusions: The results indicate that insulin interferes with inflammatory cytokine production by stimulated PBMC and it affects the cross talk between immune and colon cancer cells. It appears that the effect of insulin on the immune balance between mononuclear and malignant cells depends on its concentration and type of cancer cells. The findings provide and additional way for understanding the relation between insulin and cancerogenesis.