Comparative Analysis of FCGR Gene Polymorphism in Pulmonary Sarcoidosis and Tuberculosis

The clinical outcome of sarcoidosis (SA) is very similar to tuberculosis (TB); however, they are treated differently and should not be confused. In search for their biomarkers, we have previously revealed changes in the phagocytic activity of monocytes in sarcoidosis and tuberculosis. On these monocytes we found a higher expression of receptors for the Fc fragment of immunoglobulin G (Fc?R) in SA and TB patients vs. healthy controls. Fc?Rs are responsible for the binding of immune complexes (ICs) to initiate an (auto)immune response and for ICs clearance. Surprisingly, our SA patients had a high blood level of ICs, despite the abundant presence of Fc?Rs. It pointed to Fc?R disfunction, presumably caused by the polymorphism of their (FCGR) genes. Therefore, we present here an analysis of the occurrence of FCGR2A, FCGR2B, FCGR2C, FCGR3A and FCGR3B variants in Caucasian SA and TB patients, and healthy individuals with the use of polymerase chain reaction (PCR) and real-time PCR. The presented data point to a possibility of supporting the differential diagnosis of SA and TB by analyzing FCGR2C, FCGR3A and FCGR3B polymorphism, while for severe stages of SA also by studying FCGR2A variants. Additionally, the genotyping of FCGR2A and FCGR3B might serve as a marker of SA progression.

Automated summary

The clinical outcome of sarcoidosis (SA) and tuberculosis (TB) is similar, but they are treated differently. Previous research has shown changes in the phagocytic activity of monocytes in SA and TB, with a higher expression of Fc?R receptors in these patients. However, despite the presence of these receptors, SA patients have high levels of immune complexes (ICs), indicating a dysfunction in Fc?R potentially caused by FCGR gene polymorphisms. This study analyzed the occurrence of FCGR2A, FCGR2B, FCGR2C, FCGR3A, and FCGR3B variants to differentiate between SA and TB and potentially serve as markers for SA progression.