Few areas of immunologic research have endured such strident criticism
or engendered such fainthearted support as the study of antigen-speci
fic suppression of the immune response. Although enjoying a modest res
urgence as a means of promoting or maintaining peripheral tolerance to
autoantigens, the study of antigen-specific suppression is not mainst
ream immunology. The field of immune regulation has, in fact, shifted
focus toward explaining the data in terms of the Th1/Th2 paradigm. Ind
eed, the term suppression has been coopted, by those willing to use it
, to describe the bioactivity of conventional cytokines, such as IL-4,
IL-10 or TGF beta, which can be inhibitory in certain experimental mo
dels. In a very real sense, those who performed much of the early work
in the field bear responsibility for the outcast status of suppressio
n. With the increasing number of soluble mediators and cascades of int
eracting T cells, which populated reviews of the subject in the 1980s,
the concept of antigen-specific suppression and suppresser factors si
mply became too complicated and was dismissed as artifact. Several lab
oratories have in the past few years made significant advances in the
molecular characterization of antigen-specific TsF. Their work, as wel
l as that of our own laboratory have established certain minimal molec
ular requirements for the expression of TsF bioactivity.