The interactions of IGG & TRIM21/RO52 in human microglial cells

TRIM21/RO52 possibly affects intracellular-antigen destruction (in neurological-auto-immune diseases) by auto-antibodies and alleviating this destruction by IVIG. We investigated the time and the immune-response group (naive and 24 hr LPS-incubated (LPSI)) based changes of the IgG and TRIM21/Ro52 levels in the IgG-incubated HMC3-microglial cells with FCM and confocal-microscopy. According to the FCM results. a) In both groups, the IgG appearances were negligible until the 48th hour. b) TRIM21/Ro52 was elevated in LPSI and dropped (but raised in the naive group) in the first 20 min of IgG incubation. After 20 minutes, changes in the TRIM21/Ro52 levels were parallel in both groups, but TRIM21/Ro52 was significantly higher in LPSI (levels rose again after bottoming in the range of 60 min - 4 hr). c) Some cells became TRIM21/Ro52(-) at the 48 hr. d) The confocal microscopic views highlighted colocalization of IgG and TRIM21/Ro52 except the 48th hour in which individual and numerically more IgG areas emerged. These results suggest: time and the immune-state dependent bidirectional relation between IgG and TRIM21/RO52 in microglial cells, IgG in naive cells triggers a phasic TRIM21/Ro52 level rise, then IgG influx, IgG colocalization with TRIM21/Ro52, their destruction together and finally IgG appearance (alone) happens (in TRIM21/Ro52 deprived cells). Differently in LPSI, IgG influx starts immediately, and TRIM21/Ro52 levels were higher except in the 20th minute. It seems immune stress facilitates antibody internalization and microglial cells emerging as antibody absorbers and becoming TRIM21/Ro52, aberrant or deprived.