Differential effect of experimental diabetes on the early and late phase of contact sensitivity reaction in mice.

Contact sensitization induces two different kinds of T cells (both Ly 1) that act in sequence to produce upon challenge with antigen a classical 24-hour local skin swelling reaction. One of these cells produces an antigen-specific factor. It has been suggested that it sensitizes mast cells, similar to IgE antibody, and causes them to release vasoactive amines in the presence of antigen. This results in an early (2-hour) swelling reaction. Increased vascular permeability facilitates the entry of the second, lymphokine-producing Ly 1 cell into the site of reaction to elicit the classical 24-hour delayed-type hypersensitivity reaction. In alloxan diabetic mice, contact sensitivity reactions are reduced significantly, and our experiments show that insulin deficiency affects only the activity of the late acting, lymphokine-producing cell and leaves the factor-producing cell responsible for the early swelling reaction unaffected. Our experiments demonstrate that insulin deficiency has different effects on distinct subpopulations of T lymphocytes.

Macrophage function in alloxan-diabetic mice: expression and activity of Fc receptors.

The expression of Fc receptors (FcR) on macrophage surfaces is dependent on the in vitro insulin level. Macrophages (Mø) of alloxan-diabetic animals have more FcR and phagocytose heavily opsonized sheep erythrocytes (SRBC) better, than normal Mø. The reverse is, however, true when suboptimally opsonized SRBC are used. No differences were found between normal and diabetic macrophages in the rate of catabolism of engulfed antigen. We regard it likely that the generation and/or transmission of Fc-dependent signal from the cell surfaces may be impaired in hypoinsulinaemic environment.