Relapsing polychondritis is a disorder of unknown cause characterized by the destruction of cartilage. To test the hypothesis that immunologic mechanisms are involved in the pathogenesis of relapsing polychondritis, we analyzed the serum of 15 patients for the presence of antibodies to cartilage. Antibodies to Type II (cartilage) collagen were found in the serum of five patients at the time of acute symptoms. No antibodies were detected either to cartilage proteoglycan or to other collagen types. The antibodies were detected at the onset of the disease and their titers appeared to correlate with severity of disease. Circulating immune complexes were also detected in the serum of these patients. Our findings support an immunologic involvement in this condition.

sus (SLE) was carried out at 9 university centers diverse in geographic, socioeconomic, and racial characteristics. The mortality and disease characteristics of the patients at study entry varied widely among centers. The survival rates from the time patients with a diagnosis of SLE were first evaluated at the participating center was 90% at 1 year, 77% at 5 years, and 71% at 10 years. Patients with a serum creatinine >3 mg/dl at study entry had the lowest survival rates: 48%, 29%, and 12% at 1, 5, and 10 years, respectively. Survival rate also correlated independently with the entry hematocrit, degree of proteinuria, number of preliminary American Rheumatism Association criteria for SLE satisfied, and source of funding of medical care. When data were corrected for socioeconomic status, race1 ethnic origin did not significantly influence survival. Survival rates varied widely at different participating institutions, generally due to differences in disease severity. Place of treatment was independently associated with survival only in the second year after study entry. Disease duration before study entry did not account for the differences in disease severity.Reports of prognosis in systemic lupus erythematosus (SLE) from single medical centers are often not comparable because of differences in the characteristics of patient populations. Because of these differences, there has been disagreement about the natural history and clinical course of SLE. Attempts to analyze literature trends (1) and to pool data from several centers (2) have provided some insights. In order to test the reliability of these insights and to assess more accurately which factors determine sur-60 1

Causes of death were examined for 1,103 systemic lupus erythematosus patients who were followed from 1965 to 1978 at 9 centers that participated in the Lupus Survival Study Group. A total of 222 patients (20%) died. Lupus-related organ system involvement (mainly active nephritis) and infection were the most frequent primary causes of death. Causes of death were similar throughout the followup period. Hemodialysis had little impact on the length of survival for patients with nephritis. Active central nervous system disease and myocardial infarction were infrequent causes of death. There were no deaths from malignancy.Despite a linear improvement in survival rates since the turn of the century (l), mortality in systemic lupus erythematosus (SLE) is still appreciable. In 1964, Kellum and Haserick (2) EUGENE V. BARNETT(3) noted 54 (36%) deaths in 150 patients who were followed prospectively for an 8-year period. Dubois et a1 (4) in 1974 reported 249 (51%) deaths among 491 patients who were followed for 13 years. Renal disease was the most common cause of death in the latter two series. Mortality rates and causes of death reflect in part the nature of each center's patient population. In order to more accurately describe the causes of death among SLE patients treated at university-affiliated centers in the United States, we have studied the causes of death in more than 4,000 patient-years of followup of 1,103 patients with SLE who were seen by members of the Lupus Survival Study Group (5).

A B S T R A C T Normal subjects given 60 mg of prednisone orally at 8:00 a.m. developed a transient lymphopenia at 2:00 p.m. To define the populations of lymphocytes affected the number and type of lymphocytes in the peripheral blood were assayed. "Late" and "early" spontaneous sheep red blood cell rosettes were used as markers for thymus-derived (T) lymphocytes and one of its subpopulations, respectively. Receptors for aggregated gammaglobulin and complement identified bursal-equivalent or bone marrow-derived (B) lymphocytes and one of its subpopulations, respectively. 6 h after administration of 60 mg of prednisone, the blood samples showed a decrease in proportion of T cells from 69.2±2.1% to 55.9±2.8% (average+SE) and an increase in B-cell proportion from 21.3±2.0% to 44.8± 4.1%. The changes of "early" rosettes and complement receptor lymphocytes also paralleled these. In all cases the absolute numbers of T cells and of B cells were decreased by prednisone. The density gradient distribution of the lymphocytes did not change after prednisone. These data indicate that both T and B lymphocytes are affected by the prednisone but that the T cell lymphopenia was more pronounced. The lymphopenia might reflect either sequestration in the marrow and/or transient arrest of recirculation. INTRODUCTIONCorticosteroids are a group of drugs commanding much attention in immunological investigations. They have profound effects on lymphocytes in steroid-sensitive species (1), including differential effects on lymphocyte subpopulations in mice and rats.