Most notably, a decrease in na?ve B lymphocytes, an expansion of the memory B-cell compartment, and an increase in plasmablasts have been consistently described (9�C12). There is evidence to suggest that improvement in disease may be correlated with a ��normalization�� of the Erlotinib
B-cell subset distribution profile to that resembling healthy state (13). This backdrop motivated us to conduct a longitudinal method validation study using a clinically feasible whole blood staining approach in well-defined populations of healthy volunteers and subjects with SLE to profile B-cell phenotypes in SLE and to characterize the variability in the measurement of various B-cell subsets. The results of this study are expected to aid the study of therapeutic agents, both marketed and investigational, for which changes to leukocyte subpopulations, and B-cell subsets in particular, are an expected effect of pharmacologic intervention. HV (n = 20) and SLE subjects (n = 42) were enrolled at Cedars-Sinai Medical Center (Los Angeles, CA) after receiving Institutional Review Board (IRB) approval. Research was carried out in compliance with the Helsinki Declaration and approved by the Cedars-Sinai Vasopressin Receptor
IRB. The criteria for all subjects included males and females between 18 and 45 years. They were known to be negative for HIV antibodies, hepatitis B surface antigen, and hepatitis C antibodies. The HV were without a history of any chronic medical disease. Patients with SLE enrolled into the study fulfilled the 1982 Revised Criteria of the American College of Rheumatology and had a diagnosis of SLE for greater than 3 months. The patients with SLE were required to have been clinically stable and on a stable pharmacologic regimen for at least 1 month prior to enrollment. Patients with active vasculitis, active CNS lupus requiring therapy, renal insufficiency (acute and chronic), uncontrolled hypertension, uncontrolled diabetes, or active infection were excluded. Patients who received cyclophosphamide or any other alkylating agent, or 100 mg/day of prednisone or equivalent in the 60 days prior to enrollment were also excluded. HV were designated GSK126 datasheet
as Group 1. For all patients with SLE, disease severity was assessed at enrollment using the SLE disease activity index (SLEDAI) and assigned to Group 2 (SLEDAI < 8) or Group 3 (SLEDAI �� 8). After enrollment, all medical therapies deemed clinically appropriate by the investigator or treating physician were permitted. For subjects in Group 2 (SLEDAI < 8), those who received cyclosporine, tacrolimus, sirolimus, leflunomide, methotrexate, mycophenolate mofetil, azathioprine, or greater than 10 mg prednisone (or equivalent) per day were excluded.