Secretion of immunoglobulin A by human milk leukocytes initiated by surface membrane stimuli.

Some of the requirements for release of immunoglobulin A (IgA) from human milk leukocytes during phagocytosis were investigated. The role of particle adherence in IgA release was studied by using an in vitro model of frustrated phagocytosis in which human milk leukocytes were incubated with latex particles too large to ingest. Release of IgA was significantly increased from control values within 30 min in these leukocytes. A similar increment in IgA release also occurred when human milk leukocytes were incubated with other surface membrane stimuli, e.g., NFMP and phorbol. No increase in IgA release was found, however, in cells incubated with zymosan-activated serum. In addition, the release of IgA was blocked by inhibitors of actin filaments (cytochalasin B) and microtubules (colchicine). Thus, IgA is released from human milk leukocytes by secretory mechanisms that are initiated by certain membrane stimuli, some of which are shared by peripheral blood neutrophils and monocytes. Because human milk leukocytes appear to be refractory to C5a or other activated complement components and are blocked by cytochalasin B, it appears that these unusual cells may be uniquely adapted to play a role in the immunologic protection of the neonate.