REGULATION OF CONTACT HYPERSENSITIVITY BY INTERLEUKIN 1O

Contact hypersensitivity (CHS) responses require the participation of T cells, along with a variety of cytokines and adhesion molecules. In the classical CHS, antigen-specific T cells are recruited to a site of antigenic challenge, where they react with antigen, release cytokines , and attract other inflammatory cells. In the mouse model of CHS, thi s reaction is elicited in sensitized mice by application of the immuno gen 4-7 d after immunization. The reaction peaks at 24 h, is slightly reduced by 48 h, and can return to normal by 72 h. This is in spite of the fact that some antigen is still present at the site of challenge. Here we examined the hypothesis that locally produced Interleukin 10 (IL-10) regulates the duration of the response. Our data show that IL- 10 protein peaked 10-14 h after antigenic challenge and returned to ba ckground by 24 h. The production of IL-10 protein corresponded with, a nd followed IL-10 mRNA transcription as detected by reverse transcript ase-polymerase chain reaction. During peak IL-10 production after anti genic challenge, it was not possible to transfer CHS with immune lymph oid cells, unless neutralizing antibody to IL-10 was given first. Addi tionally, when sensitized mice were given neutralizing anti-IL-10 anti body at the time of antigenic challenge, the duration of CHS was prolo nged well beyond the natural course of the response. Finally, we demon strate that rIL-10, when injected into the skin before antigenic chall enge, prevented the elicitation of CHS in previously sensitized mice. Taken together, our data show an important role for IL-10 in the natur al regulation of CHS responses in vivo.