Suppressor cell activity and phenotypes in the blood or tissues of patients with leprosy.

Suppressor cell activity has been demonstrated in the peripheral blood of patients with leprosy. Cells bearing the suppressor/cytotoxic phenotype have been enumerated in both peripheral blood and tissues, and microanatomical differences in tissue distribution have been observed. This first generation of studies has been characterized by considerable disagreement, a not unusual circumstance in the study of leprosy. In the case of blood suppressor cell activity, there appears to be no doubt as to its existence, but much uncertainty regarding its distribution. Concerning peripheral blood phenotypic suppressor cells, the observed differences in lepromatous and ENL patients may well reflect differences in methods used. Concerning phenotypic suppressor cells in tissue, there is no agreement as to their numbers or microanatomical distribution across the spectrum of leprosy or in its reaction states. Although these observational differences make firm conclusions impossible, this first generation of studies has provided new ways of considering old problems. For example, lepromin unresponsiveness might be a consequence of active cellular suppression. Differences in the numbers (or percentages) of the suppressor phenotype in blood or tissues of lepromatous patients with or without ENL reopens the door to the possibility of cell-mediated immune mechanisms in the pathogenesis of ENL. The identification of defective suppressor cells as important in the pathogenesis of hypergammaglobulinaemia is of interest in and of itself, but also gives rise to the possibility that other kinds of phenomena may be a consequence of defective or effete suppressor mechanisms. The observation of microanatomical differences in the distribution of the suppressor phenotype in tuberculoid and lepromatous leprosy indicates that effective or ineffective immunity might be a sequela of particular interactions between the suppressor/cytotoxic and helper/inducer phenotypes, and that these interactions merit further study. These new perspectives may be subject to experimental testing by the next generation of studies, which will surely include the techniques of clonal expansion and limiting dilution, as well as the study of interleukins 1 and 2.