T. rubrum is especially suited to survive on the skin surface. We have presented data to show how it accomplishes this. We will now combine these data with our own thoughts to speculate about how T. rubrum has adapted to the skin of human beings. We believe the organism uses several different strategies. First, many infected patients cannot elicit a cell-mediated immune response to eliminate the fungus. The reasons for this are not completely clear, but trichophytin skin tests are negative at 48 hours despite persistent, chronic, and even widespread infections. Antigens are present on T. rubrum, just as they are on other dermatophytes, but differences in antigen penetration through the skin may prevent induction of immunity. Perhaps, neonatal exposure to the fungus or to cross-reacting antigens of molds may induce tolerance by confusing antigen recognition of self vs. nonself. More likely, persistent infection induces immunologic unresponsiveness by activating specific suppressor T cells. In fact, our attempts to clone T. rubrum-specific T cells from peripherals blood have always yielded suppressor cells, and these cells even suppress proliferation of the clone itself. Second, mannans from T. rubrum probably are better able to suppress cell-mediated immune reactions than are mannans from other fungi. T. rubrum may make more mannan than do other dermatophytes, and the mannan may be a more potent immunosuppressor than are mannans from other dermatophytes. Mannan apparently works by inhibiting critical steps in antigen processing or presentation. This inhibits the immune reaction. Perhaps, mannan even can prevent induction under certain circumstances. Third, T. rubrum is not especially aggressive compared with other dermatophytes. By remaining in the stratum corneum, it may evade immune surveillance, and may evade complement and polymorphonuclear leukocytes that would attach the organism if it tried to invade into viable epidermis. Finally, T. rubrum can survive off the human body as a spore. Its life cycle apparently lets spores desquamate and, thereby, remain plentiful in many human habitats. If a spore finds a warm, moist area of skin, it can crowd out normal flora and grow within the stratum corneum. T. rubrum's ability to infect and its ubiquitous presence account for the high incidence of infections. This, plus the ability of T. rubrum to evade host defenses, accounts for the high prevalence of infections with this fungus.
|Original language||English (US)|
|Pages (from-to)||97-109; discussion 110-111|
|Journal||Advances in dermatology|
|State||Published - 1994|