Regulatory role for the immune complex in modulation of phagocytosis by 3-deazaadenosine.
The S-adenosyl-L-homocysteine hydrolase inhibitor 3-deazaadenosine (3-DAA) modulates antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent phagocytosis (AD phi) by mouse spleen effector cells and antibody-coated erythrocyte target cells. Concentrations of this compound inhibiting ADCC caused augmentation of phagocytosis. In a modified version of these assays referred to as complement-independent cellular cytotoxicity (CICC) and complement-independent phagocytosis (CI phi), specifically immune spleen cells were the source of effector cells and antitarget antibodies. CICC and CI phi were assayed with antiserum-untreated erythrocyte target cells. Although CICC was inhibited, 3-DAA failed to induce augmentation of phagocytosis in CI phi assays. Augmentation was restored by the presence of antibody-coated targets. If 3-DAA was present before the initiation of the assay by the addition of antibody-coated targets, it also failed to augment conventional AD phi. Varying dilutions of the antiserum, used for the preparation of antibody-coated target cells, induced differential effects of 3-DAA on phagocytosis. A regulatory interaction between the target cell antigen-antibody complex and the action of 3-DAA on phagocytosis has been suggested.[1]References
- Regulatory role for the immune complex in modulation of phagocytosis by 3-deazaadenosine. Medzihradsky, J.L. J. Immunol. (1984) [Pubmed]
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