Recruitment of immature neutrophils in peripheral blood following leukocytapheresis therapy for rheumatoid arthritis

Abstract

The objective of this study is to evaluate the cellular mechanism underlying filtration leukocytapheresis (LCAP) therapy for the treatment of rheumatoid arthritis (RA). Thirteen patients with refractory RA each underwent three sessions of LCAP. Before (pre-) and after (post-) the completion of the first LCAP session, peripheral blood was sampled and analyzed for neutrophil surface markers using flow cytometry. The surface antigens of peripheral blood mononuclear cells (PBMCs) and neutrophils obtained at pre- and post-LCAP were then analyzed using a fluorescence-activated cell sorter. The American College of Rheumatology's criterion of a 20% improvement was achieved in six patients, but not in the other seven patients, after LCAP therapy. The post-LCAP number of blood band form neutrophils with a bone marrow phenotype (CD49d(dim+), low density) was higher among the responders than among the nonresponders, suggesting an association between the clinical response and the recruitment of bone-marrow-derived neutrophils. After the nonspecific absorption of WBCs during a 1-h Cellsorba procedure, the number of PBMCs was consistently decreased, although the number of neutrophils that were affected by removal plus recruitment varied in a manner that was independent of efficacy. In contrast, the emergence of immature neutrophils in the peripheral blood was characteristic of the effective therapies. These cells were found after the 1st session of responders and also found following sessions of LCAPs. Immature neutrophils, which may be recruited from the bone marrow in the peripheral blood after the first session of LCAP, can predict the clinical efficacy of subsequent LCAP sessions.

Induction of Foxp3 expression in T cells by cellulose acetate beads in vitro

“…Recently, granulocyte and monocyte apheresis (GMA) has been established as an effective therapy for IBD [8] and is also expected to be a useful therapy for rheumatoid arthritis [9,10].…”

Leishmania major Strain-Dependent Macrophage Activation Contributes to Pathogenicity in the Absence of Lymphocytes

“…Both are proinflammatory markers, and their expression is induced robustly under inflammatory conditions ( 30 , 31 , 50 ). Although it has been reported that L. major can promote the M2 macrophage to support their growth ( 43 , 44 ), no significant differences were observed in CD206 expression between 5-ASKH and FV9, the markers of the M2 macrophage. Collectively, these data suggest that 5-ASKH activates CD11b + Ly6G − F4/80 + macrophages rather than FV9, which seems to initiate the neutrophil recruitment process.…”