Changed phagocytic activity and pattern of Fcγ and complement receptors on blood monocytes in sarcoidosis.

Abstract We have recently revealed that mycobacterial heat shock proteins (Mtb-hsp), involved in forming of immune complexes (CIs), can induce immune response in sarcoidosis (SA). The complexemia may result from inappropriate phagocytosis and clearance of CIs by monocytes with following persistent antigenemia and granuloma formation. Because an aberrant expression of receptors for Fc fragment of immunoglobulin G (FcγR) and complement receptors (CR) on monocytes can be involved in this process, we have evaluated the expression of FcγRI (CD64), FcγRII (CD32), FcγRIII (CD16) and CR1 (CD35), CR3 (CD11b), CR4 (CD11c) receptors on blood CD14 + monocytes and its phagocytic activity in 24 patients with SA and 20 healthy volunteers using flow cytometry. We found significantly increased expression of all examined FcγR and decreased expression of CD35 and CD11c on CD14 + monocytes in SA patients vs controls. Significantly increased percentage of CD14 + CD16 + CD35 − , CD14 + CD64 + CD35 + , CD14 + CD64 + CD11b + , CD14 + CD64 + CD11c + and decreased of CD14 + CD32 − CD35 + , CD14 + CD32 − CD11b + , CD14 + CD32 − CD11c + monocytes’ phenotypes was revealed in SA. The total number and percentage of phagocyting monocytes was significantly increased in SA as compared with controls. In conclusion, altered expression of FcγR and CR on CD14 + monocytes and its increased phagocytic activity may be responsible for high antigen load, persistent antigenemia and immunocomplexemia in SA patients.