1. Top of page
  2. Abstract
  6. Acknowledgements


To evaluate the safety and efficacy of a humanized monoclonal antibody against CD154 (IDEC-131) in patients with active systemic lupus erythematosus (SLE).


In this phase II, double-blind, placebo-controlled, multiple-center, multiple-dose study, 85 patients with mild-to-moderately active SLE were randomized to receive 6 infusions of IDEC-131, ranging from 2.5 mg/kg to 10.0 mg/kg, or placebo over 16 weeks. Efficacy was assessed at week 20, primarily by the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) and secondarily, by multiple measures of disease activity. Safety was assessed through week 28 by clinical and laboratory evaluation. Immunogenicity studies were also performed.


SLEDAI scores improved from the baseline levels of disease activity in all groups, including the placebo group. However, these scores were not statistically different among the IDEC-131 treatment and placebo groups at week 20. Evaluations of secondary variables did not indicate significant differences between the IDEC-131 treatment and placebo groups. The type and frequency of adverse events were similar between the IDEC-131 and placebo groups.


IDEC-131 administered at doses ranging 2.5–10.0 mg/kg over 16 weeks was safe and well tolerated in patients with SLE. Efficacy of the drug compared with placebo was not demonstrated. There were statistically significant improvements from baseline in all groups, including the placebo group.

Systemic lupus erythematosus (SLE) is a chronic, multisystem autoimmune disease associated with immune system dysfunction and characterized by the production of autoantibodies to nuclear antigens (1). A consistently observed manifestation of immune dysfunction in SLE is the hyperactivity of the humoral immune system, both in vitro and in vivo (2). Recent observations in murine lupus models have led to the development of new strategies in the treatment of humans with SLE (3, 4). One strategy is based on the observation that the activation of T lymphocytes requires at least 2 signals. The first signal is provided when antigen is presented to the T cell receptor in the context of the class II molecules on antigen-presenting cells (APC). The second signal is provided by receptor–ligand pairs on T lymphocytes and APC (5, 6). An important example is the interaction between CD40 on APC and its ligand (CD40L or CD154) on T lymphocytes. CD40 is expressed on APC and many other cell types, including B lymphocytes (7). CD154 is found predominantly on activated CD4+ T lymphocytes (8, 9). The CD40–CD154 interaction between B and T cells promotes T cell activation and drives B cell cycle entry and differentiation. Gene-knockout studies demonstrate that there is no compensatory mechanism to replace CD154 function (10).

Recent studies in mice and in humans suggest that CD40–CD154 interactions may contribute to SLE. For example, in murine models of SLE, selective blockade of the interaction between CD40 and CD154 retards lupus nephritis and prolongs survival (4). This finding is reinforced by studies in humans demonstrating that the absolute number of CD154+ T cells is increased in patients with active SLE (2, 11, 12). After in vitro activation, T cells from patients with SLE show significantly prolonged expression of CD154 compared with T cells from normal subjects (2). Patients with active SLE have significantly higher levels of soluble CD154 in vivo compared with healthy controls (13), and soluble CD154 may mediate B cell activation in SLE patients (14). Control of the normal immune system may be dependent on minimizing expression of CD154, whereas persistent expression of CD154 may disrupt this control, leading to autoimmunity (8, 15). These observations support the hypothesis that blockade of the CD40–CD154 interaction may exert control over established abnormal responses such as those in SLE.

IDEC-131 is a humanized monoclonal antibody against CD154, comprising human γ1 heavy chains and human κ light chains with murine complementarity/determining regions. It does not activate T cells, endothelial cells, or platelets, and it does not up-regulate tissue factor (15, 16). In a phase I trial, IDEC-131 was well tolerated in 23 patients with SLE, at single doses of 0.05 mg/kg to 15.0 mg/kg (17).

The present study was designed to examine the safety and efficacy of multiple doses of IDEC-131 (2.5, 5.0, or 10.0 mg/kg) compared with placebo in patients with active SLE. The dosing levels were based on in vivo studies in nonhuman primates, which demonstrated that a weekly dose of 5.0 mg/kg of IDEC-131 for 8 weeks inhibited the immune response to ovalbumin at circulating plasma levels expected for the current study.


  1. Top of page
  2. Abstract
  6. Acknowledgements

Study design.

The study was a phase II, double-blind, placebo-controlled, multicenter, dose-comparing clinical trial of IDEC-131 in patients with active SLE. Informed consent was obtained from all patients in accordance with the human subjects institutional review boards of each of the participating centers. Patients were treated for 16 weeks; each patient received single 1-hour intravenous infusions of 2.5, 5.0, or 10.0 mg/kg of IDEC-131 on weeks 0, 2, 4, 8, 12, and 16 in an outpatient clinical setting. Patients assigned to the placebo group received a 250 ml solution of normal saline. Efficacy assessments were determined at baseline (week 0), at each treatment visit, and at 1 posttreatment followup visit (week 20; 4 weeks after the last infusion). Several efficacy outcome instruments were utilized. Patients were evaluated over the treatment and followup periods to assess pharmacokinetics, toxicity, and effects on peripheral blood lymphocytes, serum chemistry levels, complement levels, anti–double-stranded DNA (dsDNA) antibodies, and erythrocyte sedimentation rates.

Patient selection.

Study patients were required to fulfill the criteria for the classification of SLE as defined and revised by the American College of Rheumatology (18, 19). Inclusion criteria included an age of at least 18 years, the presence of antinuclear antibodies at study entry or in the past, mild-to-moderately active disease as defined by a score of 4–12 on the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) scale, as modified by the Safety of Estrogen in Lupus Erythematosus National Assessment (SELENA) study (20), disease duration for ≥6 months at study entry, and specified therapy for SLE that had been stable for 8 weeks prior to study entry. Patients were excluded from the study if they had prior treatment with a monoclonal antibody or other biologic agents. Patients with a history of recurrent or active infection, including human immunodeficiency virus, or another clinically significant condition were also excluded.

Primary efficacy variable.

SELENA SLEDAI. The SELENA SLEDAI, a validated instrument that measures SLE disease activity within the month prior to assessment (20), was the primary outcome variable for the study. Baseline scores were compared across treatment groups, using an analysis of variance with treatment group as the only factor. Within-group change from baseline to week 20 was analyzed using a paired t-test. Mean change from baseline to week 20 was compared across treatment groups using an analysis of covariance (ANCOVA) model adjusted for baseline SELENA SLEDAI scores. The primary efficacy analysis was the ANCOVA analysis at week 20.

Secondary efficacy variables.

British Isles Lupus Assessment Group (BILAG) Index.

Using the BILAG Index, a validated instrument that measures SLE activity from the perspective of the intention to make a treatment change (21), the categories (worsening, present, improving, resolved) were determined at each assessment. At the baseline visit, if disease activity was present in any category, it was recorded as present regardless of whether the clinical variable was worsening, improving, or stable.

Physician global assessment.

At each assessment, the investigator described overall SLE disease activity for each patient on an indexed 5-cm visual analog scale (VAS), with 0 noted on the scale as no disease activity and 3 noted as severe disease activity.

Patient global assessment.

Patients assessed their SLE disease activity at each assessment on a 10-cm VAS, ranging from 0 (worst ever) to 10 (best ever).

Time to flare.

The time to disease flare was defined as the number of days from the first infusion to the first assessment of mild/moderate or severe flares of the disease. The SELENA SLEDAI flare definitions were used as previously described (22).

Krupp fatigue assessment.

Using the Krupp fatigue severity scale, patients noted their degree of agreement for 9 fatigue-related statements, ranging from 1 (strongly disagree) to 7 (strongly agree), as previously described (23). Values were averaged to produce a global score, ranging from 1 (low fatigue severity) to 7 (high fatigue severity).

Anti-dsDNA antibody and serum complement.

Samples for anti-dsDNA antibody and serum complement (CH50, C3, and C4) studies were processed by Covance Central Laboratory Services (Indianapolis, IN). Anti-dsDNA titers were measured using the NEN Life Science Products Anti-dsDNA I-125 Radiobinding Assay, based on the Farr assay. Complement C3 and C4 concentrations were measured using a Beckman Image Protein System nephelometer (Beckman Instruments, Brea, CA). Total complement (CH50) activity was measured using a hemolytic assay manufactured by Diamedix Corporation (Miami, FL).

Medical Outcomes Study (MOS) Short Form 36 (SF-36) health survey.

The SF-36 survey, which has been validated as a measure of quality of life for SLE patients (24), was performed at each visit.

Evaluation of safety.

Patients were followed up with a variety of safety assessments throughout the treatment period and up to week 28.

Adverse events.

Treatment-emergent adverse events were defined as adverse events that were first reported following initiation of study treatment, or adverse events that worsened in severity or in relationship to the study drug.

Laboratory studies.

Standard methods were used for hematology, blood chemistry, and urinalysis studies. A central laboratory (Covance) was utilized for all laboratory studies.

Lymphocyte subsets.

Flow cytometry assays were performed to measure lymphocyte populations, including CD3-, CD4-, CD8-, and CD19-positive subsets (IDEC Pharmaceuticals Clinical Immunology Laboratory, San Diego, CA).


Serum levels of anti–IDEC-131 antibody were determined at baseline and at weeks 20 and 28 by a validated enzyme-linked immunosorbent assay (IDEC Pharmaceuticals Clinical Immunology Laboratory).


  1. Top of page
  2. Abstract
  6. Acknowledgements

Patient disposition and population.

Eighty-five patients from 11 centers in the United States and 1 site in Canada were randomly assigned to 1 of 4 treatment groups: 19 patients to the 2.5 mg/kg IDEC-131 dose group, 22 patients to the 5.0 mg/kg IDEC-131 dose group, 24 patients to the 10.0 mg/kg IDEC-131 dose group, and 20 patients to the placebo group. Patient demographics and organ system involvement are summarized in Tables 1 and 2, respectively. Of the 85 patients, 67 (79%) completed the study. Reasons for premature withdrawal were predominantly adverse events, a lack of efficacy, or use of prohibited medication. Adverse events leading to withdrawal included hip replacement, migraine, dysuria, recurrent Ménière's syndrome, herpes zoster, pruritus, rash, and a single event of malignancy (bronchioloalveolar carcinoma of the lung).

Table 1. Patient characteristics and systemic lupus erythematosus status at baseline (n = 85)*
Characteristic*IDEC-131, mg/kgPlacebo (n = 20)
2.5 (n = 19)5.0 (n = 22)10.0 (n = 24)
  • *

    ACR = American College of Rheumatology. SELENA SLEDAI = Safety of Estrogen in Lupus Erythematosus National Assessment–Modified Systemic Lupus Erythematosus Disease Activity Index.

  • Time since date of original diagnosis of systemic lupus erythematosus to date of study entry.

Age, years    
Sex, no. female/male19/022/022/219/1
Race, no. (%)    
 Caucasian9 (47.4)11 (50.0)13 (54.2)10 (50.0)
 African American7 (36.8)8 (36.4)8 (33.3)3 (15.0)
 Hispanic2 (10.5)1 (4.5)3 (12.5)4 (20.0)
 Asian1 (5.3)2 (9.1)0 (0.0)1 (5.0)
 Other0 (0.0)0 (0.0)0 (0.0)2 (10.0)
Time since first diagnosis, months    
Total no. of ACR criteria met    
Table 2. Patients with specific organ involvement at study entry*
Organ systemIDEC-131, mg/kgPlacebo (n = 20)
2.5 (n = 19)5.0 (n = 22)10.0 (n = 24)
  • *

    Values are the number (%) of patients.

Mucocutaneous18 (95)17 (77)23 (96)17 (85)
Musculoskeletal16 (84)17 (77)23 (96)20 (100)
Neurologic5 (26)3 (14)4 (17)4 (20)
Cardiovascular/ Respiratory7 (37)7 (32)10 (42)9 (45)
Vasculitis4 (21)3 (14)6 (25)7 (35)
Renal6 (32)6 (27)8 (33)4 (20)
Hematologic11 (58)11 (50)14 (58)9 (45)

Efficacy of treatment.


At week 20, the mean change from baseline total SLEDAI scores indicated improvement in disease activity within each treatment group (Table 3). No significant differences were found among the IDEC-131 treatment and placebo groups. No dose-response relationship was noted. An analysis using a time-adjusted area under the curve minus baseline values for the SELENA SLEDAI scores was also calculated at week 20. Results did not differ among the IDEC-131 treatment and placebo groups, and no dose-response relationship was noted at week 20.

Table 3. SELENA SLEDAI total score and change from baseline to week 20*
VisitIDEC-131, mg/kgPlacebo
  • *

    See Table 1 for definitions.

  • P = 0.371 versus placebo at baseline, by one-way analysis of variance.

  • P = 0.938 versus placebo for adjusted change from baseline, by analysis of covariance.

  • §

    P = 1.000 versus placebo in pairwise comparisons of change from baseline, by least significant difference method.

  • P values from paired t-test, comparing week 20 with baseline.

Day 1 (baseline)    
 No. of patients19222420
 SLEDAI score    
  Range4 to 124 to 124 to 124 to 12
Week 20    
 No. of patients16181615
 SLEDAI score    
Change from baseline    
 Range−8 to 4−8 to 4−8 to 4−8 to 4

The median global BILAG scores at week 20 indicated a reduction in SLE activity; however, these results were not significantly different among treatment and placebo groups (data not shown). The most commonly involved systems at baseline were mucocutaneous and musculoskeletal. The baseline BILAG scores for these 2 systems were similar among the IDEC-131 treatment and placebo groups, and week 20 results were similar to baseline. The remaining organ systems showed similar results.

Physician global assessment.

An improvement in patients' disease activity was indicated by physician global assessment on 5-cm VAS for all groups at week 20. However, the mean change in scores from baseline to week 20 was not statistically different between the treatment groups and the placebo group (data not shown).

Patient global assessment.

Mean baseline scores on the 10-cm VAS for patient global assessment in the 2.5, 5.0, and 10.0 mg/kg groups were 4.29, 5.10, and 5.16, respectively, and 5.16 for the placebo group. The mean change in scores from baseline to week 20 ranged from −0.19 to 0.68 in the IDEC-131 treatment groups and was 0.06 for the placebo group. However, none of these changes was statistically significant (P = 0.571).

Time to flare.

Fifty-seven patients experienced mild/moderate or severe flares of disease activity during the study, among whom 14 (74%) were in the 2.5 mg/kg group, 17 (77%) in the 5.0 mg/kg group, 13 (54%) in the 10.0 mg/kg group, and 13 (65%) in the placebo group; severe flares in the respective dose groups occurred in 3 patients (16%), 5 patients (23%), none of the patients, and 2 patients (10%), respectively. The median times to flare in the 2.5, 5.0, and 10.0 mg/kg groups were 113, 71, and 158 days, respectively, and 85 days for the placebo group (P = 0.549). Survival curves, using the Kaplan-Meier product-limit estimate for time to flare as measured from the day of first infusion, are presented in Figure 1 by treatment group. Time to flare between treatment groups was compared using the log-rank test. P values comparing each treatment group with placebo were not significant.

thumbnail image

Figure 1. Probability of time to flare. Kaplan-Meier estimates of the distribution of time to flare up of systemic lupus erythematosus were derived and plotted by treatment group (2.5–10.0 mg/kg IDEC-131 or placebo).

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Krupp fatigue assessment.

Mean baseline scores for the Krupp fatigue assessment in the 2.5, 5.0, and 10.0 mg/kg groups were 5.27, 5.08, and 5.35, respectively, and 5.21 for the placebo group. Mean change from the baseline to week 20 scores ranged from −0.34 to 0.37 for the IDEC-131 treatment groups and was 0.13 for the placebo group. Week 20 scores were not significantly different among the IDEC-131 treatment and placebo groups (P = 0.193).

Anti-dsDNA antibody and serum complement.

The changes in levels of anti-dsDNA antibody and serum complement were not statistically significant in any group or between treatment groups and placebo (Table 4). Of the 85 patients in the study, only 17 had clinically significant levels of anti-dsDNA antibody (≥15 IU/ml) at baseline.

Table 4. Anti–double-stranded DNA (dsDNA) antibody levels with percentage change from baseline
VisitIDEC-131, mg/kgPlacebo
  • *

    P = 0.536 versus placebo, by one-way analysis of variance.

  • P = 0.381 versus placebo, by analysis of covariance.

  • P = 1.000, P = 0.613, and P = 0.957 for 2.5, 5.0, and 10.0 mg/kg versus placebo, respectively, in pairwise comparisons of change from baseline, by least significant difference method.

  • §

    P values from paired t-test, comparing week 20 with baseline.

Day 1 (baseline)    
 No. of patients19222420
 Anti-dsDNA level, IU/ml    
  Range1.8 to 109.81.8 to 350.21.8 to 694.51.8 to 85.5
Week 20    
 No. of patients16181715
 Anti-dsDNA level, IU/ml    
Change from baseline, %    
 Range−62.3 to 547.9−51.1 to 38.9−73.1 to 40.0−66.1 to 400.0
MOS SF-36 health survey.

The physical functioning scores were similar across all groups at baseline. At week 20, the mean physical functioning scores for all groups ranged from 40.3 to 53.6 and the mean change from baseline ranged from 0.6 to 7.3. This shows an improvement in completing physical activities; however, the adjusted mean changes from baseline scores were not statistically different among the treatment groups.

Safety of treatment.

Adverse events.

Fifty-nine of 65 patients (91%) in the IDEC-131 treatment groups and 19 of 20 patients (95%) in the placebo group experienced a total of 544 adverse events. The type and incidence of the most common adverse events were similar in the IDEC-131 and placebo groups (Table 5). Treatment-related (events considered possibly or probably related, or of unknown relationship to the treatment) adverse events were reported for 43 of 65 patients (66%) in the combined IDEC-131 group and for 15 of 20 patients (75%) in the placebo group. The type and frequency of related adverse events were similar between the IDEC-131 and placebo groups.

Table 5. Incidence of common adverse events*
 IDEC-131 (n = 65)Placebo (n = 20)
  • *

    Values are the no. (%) of patients. Incidence is in ≥5% of patients, by descending frequency, in the combined IDEC-131 group or placebo group.

Headache16 (24.3)8 (40)
Nausea14 (21.5)5 (25)
Upper respiratory infection13 (20)5 (25)
Abdominal pain13 (20)5 (25)
Arthralgia10 (15.4)5 (25)
Urinary tract infection9 (13.8)2 (10)
Diarrhea8 (12.3)4 (20)
Vomiting8 (12.3)2 (10)
Dyspnea6 (9.2)1 (5)
Back pain6 (9.2)3 (15)
Sinusitis6 (9.2)1 (5)
Chest pain5 (7.7)1 (5)
Migraine5 (7.7)0 (0)
Pain in limb5 (7.7)1 (5)
Fatigue5 (7.7)2 (10)
Dermatitis4 (6.2)1 (5)
Depression4 (6.2)1 (5)
Bronchitis4 (6.2)0 (0)

Of 13 patients with serious adverse events, the events resolved or were controlled in 10. The 3 patients with ongoing events experienced unrelated events of ovarian cyst (placebo group), lower limb edema and dyspnea (placebo group), and vomiting and renal failure (10 mg/kg treatment group). Three patients experienced serious adverse events possibly related to IDEC-131: 1 patient with grade 3 bronchitis, 1 patient with grade 2 nausea and headache, and 1 patient with grade 2 migraine headaches. Notably, 1 patient in the 10 mg/kg dose group, who had a 40 pack-year smoking history and long-standing migraine headaches with associated visual symptoms, was diagnosed with a bronchioalveolar carcinoma on study day 104 and experienced a complicated migraine with ischemic cerebral infarction on day 118 while hospitalized for postbronchoscopy pneumonia. Evaluation including echocardiogram, carotid duplex scan, and serologic studies for anti-phospholipid syndrome demonstrated no evidence of a thromboembolic etiology for this event.

Laboratory studies.

No adverse trends were apparent over the course of the study for hematology, chemistry, or urinalysis study results.

Lymphocyte subsets.

Assay results for lymphocyte subsets at weeks 20 and 28 were compared with baseline values, and no significant changes were noted after IDEC-131 administration. There were no differences in the distribution of lymphocytes between the placebo and IDEC-131 treatment groups.


All patients tested negative at baseline for anti–IDEC-131 antibodies. An anti–IDEC-131 response did not develop in any of the tested patients.


  1. Top of page
  2. Abstract
  6. Acknowledgements

The objectives of this phase II, double-blind, placebo-controlled, multiple-dose study of IDEC-131 were to evaluate safety, efficacy, and immunogenicity. Due to the complicated nature of SLE, several efficacy variables were evaluated. Although SELENA SLEDAI scores improved in all treatment groups, no significant differences were noted between treatment and placebo groups at week 20. Patients treated with either IDEC-131 or placebo did not show significant changes in more objective secondary measurements, such as anti-dsDNA antibody levels; however, only 17 of 85 patients had clinically significant levels of anti-dsDNA antibody at baseline.

Of 24 patients in the 10.0 mg/kg dose group, 13 (54%) experienced disease flares, none of which was severe. In comparison, 65% of patients in the placebo group experienced flares, 10% of which were severe. In the lower dose groups (2.5 mg/kg and 5.0 mg/kg), 74% and 77%, respectively, experienced flares, of which 16% and 23%, respectively were severe. The lower incidence of flares, especially severe flares, in the 10.0 mg/kg dose group relative to placebo, although not statistically significant, may be suggestive of clinical activity of IDEC-131. This observation would require confirmation in a larger study powered for this end point.

An overall favorable safety profile was demonstrated at all dose levels examined. Adverse events experienced by patients who received IDEC-131 were similar to those experienced by the placebo group, suggesting that events were not related to IDEC-131 or were due to lupus disease activity. There were no adverse events reported that resembled an infusion-related syndrome (i.e., symptoms such as fever, chills, urticaria, and/or cardiopulmonary reactions), which has been observed with some other therapeutic antibodies. Although risk of infection could potentially be increased by blocking the CD154–CD40 pathway, only nonopportunistic infections, such as upper respiratory infections, were seen in this study, and the incidence was similar in the IDEC-131 and placebo groups.

Previous studies using a different anti-CD154 monoclonal antibody have raised serious concern that thromboembolic events may be a complication of this form of treatment (25). In contrast, no definite thromboembolic events were detected in this study. Differences in the patient populations and/or the dose of anti-CD154 may account for the absence of thromboembolic events, or alternatively, the apparent differences in the incidence of such complications may reflect intrinsic biologic differences among anti-CD154 monoclonal antibodies. In preclinical in vitro studies, IDEC-131 did not stimulate cytokine production, induce significant T cell proliferation, or activate platelets or endothelial cells. These results suggest that IDEC-131 may not up-regulate tissue factor and potentiate procoagulant activity (15, 16). Further studies will be required to definitively establish the safety of IDEC-131 in this respect and to determine the basis for the relative freedom from thromboembolic complications in this study.

No important differences were found in laboratory abnormalities between treatment groups, and lymphocyte depletion was not observed. No patient treated with IDEC-131 developed a detectable immune response to the administered monoclonal antibody. This observation suggests that patients treated with IDEC-131 can receive repeated treatments without developing an antibody response.

This phase II study did not demonstrate efficacy of IDEC-131 in patients with active SLE. There are several possible interpretations for this result. First and foremost, despite promising results from murine models, it is possible that anti-CD154 will prove to be ineffective for the treatment of SLE. However, several confounding factors must also be considered, including the high placebo response observed, the limitations of currently available disease activity indices, the population studied, the dose of anti-CD154, and the duration of the study.

High placebo-response rates have been observed in a study evaluating dehydroepiandrosterone treatment for SLE, in which a placebo response rate of 46% was noted (26). The lack of a robust responder index for global disease activity in SLE patients is a serious limitation when designing clinical trials. Due to the diversity of clinical features and the relapsing–remitting course of disease in SLE patients, it is difficult to establish a single instrument to evaluate change in disease status. None of the current validated disease activity indices was designed as an adequate responder index for evaluation of therapies for SLE. The choice to study patients with heterogeneous manifestations of mild-to-moderate disease at study entry, rather than patients with more active disease or a more homogeneous patient population, may have affected the ability to detect outcome differences between patients receiving active treatment and placebo. Restricting the study to larger numbers of patients with certain subsets of disease, such as nephritis or another target organ, may have allowed detection of treatment differences. Additionally, the dosages chosen and/or the duration of treatment may have been inadequate to affect outcome. For these reasons, although the results of this early exploration of anti-CD154 were disappointing, it would be premature to conclude that this therapeutic strategy cannot be effective in SLE.


  1. Top of page
  2. Abstract
  6. Acknowledgements

The authors wish to thank Anne Larocca, PhD and Robin Weaver for expert editorial assistance. In addition to the authors, the IDEC-131 Lupus Study Group comprises the following investigators: Jill Buyon, MD, Hospital for Joint Diseases, New York, NY; Mary Anne Dooley, MD, University of North Carolina, Chapel Hill, NC; Richard Furie, MD, North Shore University Hospital, Manhasset, NY; Ellen Ginzler, MD, SUNY Health Sciences Center at Brooklyn, Brooklyn, NY; Dafna Gladman, MD and Murray Urowitz, MD, Toronto Hospital West, Toronto, Ontario, Canada; Michelle Petri, MD, Johns Hopkins Medical Center, Baltimore, MD; Lisa Sammaritano, MD, Hospital for Special Surgery, New York, NY; Daniel Wallace, MD, Wallace Rheumatic Study Center, Los Angeles, CA; Craig Wiesenhunter, MD, Coeur d'Alene Arthritis Clinic, Coeur d'Alene, ID; and Richard G. Lizambri, MD, IDEC Pharmaceuticals, San Diego, CA.


  1. Top of page
  2. Abstract
  6. Acknowledgements
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