Sodium periodate treatment modulates the accessory and regulatory functions of alveolar macrophages in T-cell responses.

It is known that murine alveolar macrophages function inefficiently as antigen-presenting cells for the in vitro activation of macrophage-depleted T-lymphocyte populations and that they suppress antigen-stimulated lymphoproliferative responses in a dose-dependent manner. The present studies were carried out to determine whether oxidation of the alveolar macrophage surface could alter these activities. Viable alveolar macrophages were treated with varying concentrations of sodium periodate then cultured with either unfractionated or adherent cell-depleted lymphocyte populations obtained from BCG-immunized animals and challenged with PPD. It was demonstrated that moderate oxidation of the alveolar macrophage surface with sodium periodate abrogated their ability to suppress antigen-stimulated proliferation of unfractionated lymphocyte populations, as well as resulted in initiation of lymphoproliferation in an antigen-stimulated, adherent cell-depleted spleen cell populations. It is conceivable that mild oxidation of the alveolar macrophage membrane results in a more favorable interaction between the alveolar macrophage and responding T-lymphocytes, thereby reversing the alveolar macrophage-mediated suppression of antigen-stimulated lymphoproliferation and allowing for effective antigen-presenting function of these cells.