Neutralizing anti-IL-10 antibody upregulates the induction and elicitation of contact hypersensitivity.

Various cytokines have been shown to modulate the acquisition and expression of delayed-type hypersensitivity. In a mouse model, we tested the notion that neutralization of interleukin-10 (IL-10), a cytokine that inhibits T cell-mediated reactions, would upregulate delayed-type hypersensitivity. We used two different monoclonal antibodies with specificity for murine IL-10 and used allergic contact dermatitis as a prototypical example of delayed-type hypersensitivity. When anti-IL-10 antibody was given at the time of sensitization to a contact allergen, there was a substantial increase in the induced contact hypersensitivity (CHS). In other experiments, the challenge reactions to contact allergen in routinely sensitized mice were increased when anti-IL-10 antibody was given at the time of challenge. Primary irritant reactions to croton oil were increased but only if anti-IL-10 antibody was given at the time of challenge and not when it was given a week previously. It appears that anti-IL-10 antibody can potentiate CHS reactivity by inactivating otherwise downregulating endogenous IL-10.