We have previously presented evidence that the polymorphism of the FCGR3A gene, encoding the receptor for Fc fragment of immunoglobulin G IIIa (FcγRIIIa) plays a role in the enhancement of circulating immune complexes (CIs) with the occurrence of Mycobacterium tuberculosis heat shock proteins in patients with sarcoidosis (SA).
We found that FCGR3A CNVs were significantly associated with sarcoidosis in females (CN = 1 vs. CN = 2 logistic regression adjusted for sex and race, OR 4.0156, SE = 2.2784, P = 0.0143; CN = 3 vs. CN = 2 logistic regression adjusted for sex and race, OR 2.8044, SE = 1.1065, P = 0.0090), suggesting that FCGR3A gene abnormality influences sarcoidosis development in a gender-specific manner.
Thus, V158F polymorphism of FCGR3A may explain the immunocomplexemia in our patients and might serve as prognostic marker of clinical course of sarcoidosis.
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.