Lymphocytes, together with monocytederived macrophages, are common par-ticipants in inflammatory responses as-sociated with various forms of tissue injury, ranging from normal wound repair to the inflammatory-fibroproliferative response associated with the advanced lesions of atherosclerosis. Until rela-tively recently, the association of both CD4+ and CD8+ T lymphocytes with these various inflammatory-fbroprolif-erative responses, although noted by nu-merous investigators, has remained poorly understood (1-4). In some instances, it has been assumed that the presence of T lymphocytes signifies some form of immune response in asso-ciation with the tissue injury. Thus, T cells may enter the lesion in response to plaque neoantigens against which the in-dividual has not yet acquired tolerance (4). On the other hand, it has been sug-gested that their presence may simply reflect a nonspecific association. Unlike monocyte-derived macro-phages, the principal function of T lymphocytes hasnot been considered to be phagocytic or secretory, but rather to be to produce limited numbers of secreted molecules, and primarily to be involved in cell-cell interactions. Substances such as y-interferon and, more recently, several cytokines have been thought to represent the limitedrepertoire of molecules potentially formed by T cells. In the report by Blotnick et al.(5), appearing in this issue, convincing evidence is pre-sented to demonstrate that T cells pro-duce two relatively potent growthregulatory molecules-namely, some form of heparin-binding epidermal growth factor-like growth factor (HB-EGF), an apparently secreted form of basic fibroblast growth factor (FGF), a molecule which does not normally have a signal sequence and, thus, is not thought to besecreted by the classical secretory pathway. Although it is not clear that the form of basic FGF released by the T lymphocytes demonstrated in thisstudy is similarto several of the known forms of FGF that do have signal peptides, the secretion oftwo such potent growth fac-tors adds a new dimension to the poten-tial role of T lymphocytes not only as components ofthe immune inflammatory response but also as, perhaps equally important, antecedents of the fibroproliferative response associated with inflammation. The production of growth-regulatory molecules and cytokines by T cells clearly affords opportunities for T cell-nonimmune cell interactions. In the case of atherosclerosis, both CD4+ and CD8+ T lymphocytes have been shown to be common components of all phases of the lesions present, not only in experimental animals, such as nonhuman primates, but in human lesions in every stage of development (1, 4). Unlike the lesions of atherosclerosis associated with graft rejection after heart transplant, which are symmetrical and contain extraordinarily large numbers of both types of T lymphocytes as well as monocyte-derived macrophages (much greater than those found in the lesions of common atherosclerosis), thepresence of CD4+ and CD8+ cells and their possible secretory products in the lesions of common atherosclerosis raises new pos-sibilities to be considered regarding the role of T lymphocytes in the process of atherogenesis. The question of the potential antigens that may be responsible for T lymphocyte-macrophage interactions still remains unanswered. However, the role of the lymphocyte, not only in terms of its potential interactions with monocyte-derived macrophages within these inflammatory responses, but in numerous other potentially important disease processes, must now be raised in relation to the possibility thatT lymphocytes af-fect the fibroproliferative response in ways that had not …