NEUTROPHILS FROM THE SYNOVIAL-FLUID OF PATIENTS WITH RHEUMATOID-ARTHRITIS EXPRESS THE HIGH-AFFINITY IMMUNOGLOBULIN-G RECEPTOR, FC-GAMMA-RI (CD64) - ROLE OF IMMUNE-COMPLEXES AND CYTOKINES IN INDUCTION OF RECEPTOR EXPRESSION
Ja. Quayle et al., NEUTROPHILS FROM THE SYNOVIAL-FLUID OF PATIENTS WITH RHEUMATOID-ARTHRITIS EXPRESS THE HIGH-AFFINITY IMMUNOGLOBULIN-G RECEPTOR, FC-GAMMA-RI (CD64) - ROLE OF IMMUNE-COMPLEXES AND CYTOKINES IN INDUCTION OF RECEPTOR EXPRESSION, Immunology, 91(2), 1997, pp. 266-273
Neutrophils isolated from the synovial fluid of 16/24 patients with rh
eumatoid arthritis expressed Fc gamma RI (CD64), the high-affinity rec
eptor for monomeric immunoglobulin G (IgG), on their cell surface. Rec
eptor expression ranged from 17% to 168% of the level of expression ob
tained after incubation of control blood neutrophils with 100 U/ml int
erferon-gamma (IFN-gamma) for 24 hr in vitro. Similarly, mRNA for Fc g
amma RI was detected in synovial fluid neutrophils from 12/15 patients
and transcript levels ranged from 5% to 200% of the values obtained a
fter treatment of blood neutrophils with IFN-gamma for 4 hr in vitro.
No surface expression nor mRNA were detected in freshly isolated blood
neutrophils from either patients or from healthy controls. Addition o
f cell-free synovial fluid to control blood neutrophils induced both m
RNA and surface expression of Fc gamma RI to levels that were comparab
le to those achieved after addition of IFN-gamma. Neither soluble nor
insoluble immune complexes appeared to be involved in induction of Fc
gamma RI expression in spite of the ability of these complexes to indu
ce protein biosynthesis. Synovial fluid-induced expression of Fc gamma
RI was partially blocked by incubation with neutralizing IFN-gamma an
tibodies, whilst neutralizing interleukin (IL)-6 antibodies had little
effect. Levels of IFN-gamma, measured within these synovial fluids ra
nged from 0 to 2.7 U/ml, well within the range known to induce neutrop
hil Fc gamma RI expression. These data thus indicate that gene express
ion in synovial fluid neutrophils is selectively activated as the cell
s enter the diseased joint. Furthermore, these data indicate that indu
ced expression of Fc gamma RI may alter the ability of infiltrating ne
utrophils to respond to IgG-containing immune complexes present in the
se joints.