First, in line with previous reports in SLE patients,, our data indicate that ApoCell-phagocytosis is deficient in several MDM preparations that were derived from SS and SLE patients by cultivation in the absence of patients’ sera, a fact that may at least partly support a model of intrinsically defective monocyte in these disorders. Alternatively, the impaired capacity of phagocytes of SS and SLE patients for uptake of prey may be viewed as a result of cellular activation taking place in vivo, a notion probably also implied by the significant correlation between the findings in the various phagocytosis assays and the activity indices of these diseases. Finally, the notably low capacity of SS and SLE patients for phagocytosis of particulate targets by blood-borne monocytes and MDM that was observed may reflect an overall dysfunction of phagocytes in the proper engulfment of certain preys in these disorders. Interestingly, deficient phagocytosis of particulate targets is also reported in primary biliary cirrhosis, a disease with striking clinicopathologic similarities to SS. On the other hand, it should be noticed that in sharp contrast to the above deficient phagocytic capacities, the bloodborne monocytes of SS and SLE were found remarkably hyperfunctional in the phagocytosis of necrotic cell debris. The addition of healthy serum was found to facilitate significantly the ingestion of apoptotic cells by blood-borne monocytes derived from healthy individuals, as well as from SLE or SS patients. These findings are in good agreement with the previously observed capacity of sera from healthy individuals to restore the phagocytic ability of macrophages from SLE patients. In addition, ApoCell-phagocytosis by healthy monocytes was presently shown to be severely impaired following the substitution of HBD sera by sera derived from SS and SLE patients. Consistent with previous observations, the sera from approximately 80% of SLE patients studied were not as efficient as healthy sera in supporting of ApoCell-phagocytosis by normal blood-borne monocytes. In this study, we present first evidence that such incapacity is also manifested by the vast majority of sera from SS patients studied. The precise nature of this aberration in SS and SLE patients is unclear. Normally, several serum proteins attach to apoptotic cells and induce the deposition of C3 and its degradation products C3b and iC3b, thus enhancing efferocytosis by phagocytes via recognition by complement receptors CR3 and CR4. In this context, mice lacking such bridging molecules, such as MFG-e8, Mer or C1q are reported to develop lupus-like manifestations GW-572016 associated with inefficient removal of apoptotic cells. In line to these observations, several quantitative and functional aberrations of the above opsonins have been described in SLE and SS patients, including hypocomplementemia, which is considered as one of the major immunological markers and of key clinical importance for both disorders.