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Abnormal processing of immune complexes (IC) may be important in the pathogenesis of systemic lupus erythematosus (SLE). The clearance of large soluble IC (comprising hepatitis B surface antigen (HBsAg)/anti-HBsAg) radiolabeled with "23I was examined in 12 normal subjects and 10 patients with SLE. IC localization was analyzed by static and dynamic gamma-scintigraphy. Initial IC clearance from blood was more rapid in patients (median 11/2 = 2.15 min) than normals (median t1/2 = 5.15 min) due to more rapid uptake in the liver. However, in the SLE group, up to 12% of complexes were released from the liver after 30-50 min. Splenic uptake of immune complexes was reduced in the patients and there was reduced ability to retain IC in this organ. Plasma complement levels and erythrocyte complement receptor type 1 numbers were reduced in the patients, resulting in defective opsonization of IC and reduced red cell binding in vivo. These observations support the hypothesis that IC handling is abnormal in SLE. (J. Clin.

SUMMARYAn allotypic variant of Fc°RIIa, Fc°RIIa-HR (Fc°RIIa-R131), has been shown in vitro to reduce the capacity of phagocytic cells to bind and internalize IgG-containing immune complexes. Our aim was to determine whether this allotypic variant was associated with susceptibility to SLE and the development of lupus nephritis, as previous studies have suggested. Fc°RIIA genotype analysis was performed by amplification refractory mutation system-polymerase chain reaction (ARMS-PCR) in 215 Caucasoid, 70 Afro-Caribbean, and 46 Chinese patients with SLE, and in 259, 77, and 49 ethnically matched controls, respectively. Distribution of Fc°RIIa genotypes between the patients and ethnically matched controls was not significantly different in the three populations studied. No association between the Fc°RIIa-HR allotype and nephritis was found. Our results suggest that the Fc°RIIa-HR allotype is not a major factor predisposing to the development of SLE, or to lupus nephritis.

This study describes the development and validation of a brief self-report measure of emotional intelligence based on Salovey and Mayer’s (1990) conceptualization. In stage one, the 33-item Emotional Intelligence Scale (EIS: Schutte et al., 1998 ) was assessed for content validity by a panel of experts. The panel deemed 17 items unsuitable for further analysis. In stage two, a theoretically derived 5-factor solution and a unidimensional model were subjected to confirmatory factor analysis (CFA) in a student-athlete sample (n = 955). Results supported the multidimensional solution. The Brief Emotional Intelligence Scale (BEIS-10) was developed by extracting the two items from each factor with the most salient factor loadings. CFA results yielded good fit indices for the 10-item, 5-factor solution. Finally, stage three provided evidence of test-retest stability for the BEIS-10 over a 2-week period in a sample of 111 student-athletes. The BEIS-10 is offered as a valid and reliable measurement tool that has particular utility in situations where brevity is important.

C1q deficiency strongly predisposes to the development of systemic lupus erythematosus in humans and mice. We used the model of accelerated nephrotoxic nephritis in C1q-deficient mice to explore the mechanisms behind these associations. C1q-deficient mice developed severe glomerular thrombosis within 4 days of induction of disease, whereas wild-type mice developed mild injury. These findings suggest that C1q protects from immune-mediated glomerular injury. This exacerbated thrombosis was also seen in mice triply deficient in C1q, factor B, and C2, excluding a major pathogenic role for the alternative pathway of complement in this phenomenon. However, these mice did not develop elevated creatinine levels. No exacerbation of accelerated nephrotoxic nephritis was observed in mice doubly deficient in factor B and C2, suggesting a protective role for C1q against renal inflammation that is proximal to C2 activation. There were increased murine IgG deposits, neutrophil numbers, and apoptotic cells in the glomeruli of C1q-deficient mice compared with wild-type mice. Renal expression of genes encoding procoagulant proteins was also enhanced in C1q-deficient mice. The increased IgG deposits and apoptotic cells in the glomeruli of C1q-deficient mice suggest that the exacerbation of disease may be due to a defect in the clearance of immune complexes and/or apoptotic cells from their kidneys.