An experimental model to investigate orbital granuloma formation in inbred rats was established. Animals sensitized to trinitrophenyl ovalbumin (TNP-OA) and challenged retro-orbitally with TNP-OA covalently linked o Sepharose 4B beads specifically developed a granulomatous response. This granulomatous reactivity was passively transferred into normal animals by lymph node cells, but not by serum antibody from sensitized donors. Lymphocytes which transfer granuloma formation in normal recipients were characterized by cell fractionation and membrane marker analysis. These experiments show that the effector cells capable of transferring granulomatous hypersensitivity are enriched in the lower density fractions on discontinuous Percoll gradients. These cells are lymphoblasts and express the W3/25 helper T lymphocyte marker. It was also demonstrated that lymphoid cells from sensitized donors in the higher density Percoll fraction appear to be incapable of adoptively transferring granulomatous responsiveness directly to normal recipients. However, incubation of these high density lymphocytes with specific antigen resulted in marked enhancement of their ability to transfer the disease. Antigen-induced activation also resulted in an increase in both lymphoblasts and the W3/25 marker. The authors conclude, therefore, that a subset of T cells which are lymphoblasts and express the helper-cell marker is responsible for granuloma formation in sensitized animals and is capable of transferring orbital granuloma formation to non-sensitized normal recipients.