FcγR and CR on blood monocytes in differentiation between sarcoidosis and tuberculosis

Genetically different patients with sarcoidosis (SA) and tuberculosis (TB) induce dissimilar immune responses to the same mycobacterial heat shock proteins, which are implicated in forming of immune complexes (CIs). The complexemia in both diseases may result from a different function disorder of receptors for Fc of immunoglobulin G (FcγR) and complement receptors (CR) on monocytes in the phagocytosis and clearance of CIs with following persistent antigenemia and granuloma formation. Therefore, we analyzed the occurrence of FcγRI, FcγRII, FcγRIII and CR1, CR3, CR4 on blood CD14+ monocytes in 24 SA patients, 20 TB patients and 20 healthy volunteers using flow cytometry. Our results revealed significantly increased monocytes' presence with FcγRI-III and decreased with CR1 and CR4 in SA than controls. Analysis of monocytes' phenotypes revealed increased FcγRIII+CR1- and decreased FcγRII-CR1, FcγRII-CR3+, FcγRII-CR4+ occurrence in SA vs controls. In TB, higher presence of monocytes with particular FcγRI+, FcγRII+, CR1+ and CR3+ than in controls was detected. In SA vs TB, the occurrence of monocytes with FcγRIII+ receptor was significantly higher and with CR1+ was less frequent. The monocytes' phenotype FcγRIII+CR1- was increased in SA vs TB. In summary, there are increased frequencies of FcγRI+ and FcγRII+ monocytes in both SA and TB but in contrast to TB, sarcoid monocytes had increased FcγRIII occurrence with CR1 and CR4 deficiency. In SA, increased FcγR presence but CR deficiency on surface of blood monocytes may explain persistent antigenemia and complexemia in our patients with SA. This study may be useful for differentiation of both diseases.