Altered immune function in alloxan-induced diabetes in mice

Abstract

Macrophage lectin receptors that recognize bacterial cell wall sugars are reduced in alloxan diabetic mice. This is in contrast to the expression of macrophage Fc (IgG2b) receptors which remains unaltered. Peritoneal macrophages, from diabetic and normal mice, were used as a source of accessory cells in an antigen dependent T cell proliferation assay with unopsonized Staph. epidermidis as the antigen. Uptake of this antigen in the absence of serum is via the macrophage lectin receptors. We have shown that diabetic macrophages induce a level of antigen dependent T cell proliferation to Staph. epidermidis. However the T cell response to Con A was similar with both normal and diabetic macrophages. We suggest that the observed defect in antigen presentation by diabetic macrophages is at the level of uptake of antigen. High glucose levels, such as those found in diabetes, down-regulate the lectin receptor, reduce phagocytosis of Staph. epidermidis and affect antigen presentation. This has important consequences in terms of the ability of diabetics to mount an effective immune response.