Serum Proteins in Systemic Lupus Erythematosus

Attention is drawn to the difficulties that may be encountered in the positive identification and classification of many patients suspected of suffering from systemic lupus erythematosus. Much of this is due to a lack of specific criteria, either clinical or pathologic, for the diagnosis of the disease. The problem has been made more difficult by the recognition of a number of other syndromes that bear a superficial resemblance to systemic lupus erythematosus, yet differ in clinical manifestations, natural course, prognosis and other respects. A feature common to the group is the presence of the L.E. cell phenomenon. The related conditions differ from lupus enythematosus in that the L.E. phenomenon may only be demonstrable intermittently especially during severe exacerbations of the disease, while at the same time disturbances in the electrophoretic pattern of the serum proteins may be much more profound. In systemic rheumatoid disease the prognosis without steroid therapy is better than in systemic lupus erythematosus, although the morbidity may be great. The reactions which follow administration of certain chemotherapeutic agents are of considerable interest, particularly in view of the similarity to lupus erythematosus and rheumatoid arthritis, and the reversibility on withdrawal of the offending agent. The relationship of these syndromes to each other and to classical systemic lupus erythematosus has not yet been resolved, and inclusion of them under the diagnosis of systemic lupus erythematosus at this time must be regarded as premature.

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Abnormal Serum Proteins as Aids in Diagnosis of Rheumatoid Arthritis and Systemic Lupus Erythematosus

Medical Clinics of North America ◽

10.1016/s0025-7125(16)34173-6 ◽

1959 ◽

Vol 43 (2) ◽

pp. 607-613 ◽

Cited By ~ 1

Author(s):

Evan M. Barton

Keyword(s):

Rheumatoid Arthritis ◽

Systemic Lupus Erythematosus ◽

Lupus Erythematosus ◽

Serum Proteins ◽

Systemic Lupus

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Hidden autoantibodies against common serum proteins in murine systemic lupus erythematosus. Detection by in vitro plaque-forming cell assay.

Journal of Experimental Medicine ◽

10.1084/jem.161.6.1587 ◽

1985 ◽

Vol 161 (6) ◽

pp. 1587-1592 ◽

Cited By ~ 3

Author(s):

P L Cohen ◽

R G Rapoport ◽

R A Eisenberg

Keyword(s):

Systemic Lupus Erythematosus ◽

B Cell ◽

Lupus Erythematosus ◽

Cell Activation ◽

Serum Proteins ◽

B Cell Activation ◽

Systemic Lupus ◽

Autoantibody Production ◽

Murine Systemic Lupus Erythematosus

The autoantibodies found in human and murine systemic lupus erythematosus (SLE) are generally directed against cells or components of cells such as nuclear antigens. This predilection may be due to the unusual immunogenicity of certain autoantigens, or to unusual patterns of antibody crossreactivity. Alternatively, the observed spectrum of reactivities may reflect the in vivo absorption of those autoantibodies directed against soluble antigens. To test whether hitherto undetected autoantibodies against serum proteins might exist in murine SLE, we developed assays that were independent of the possibility of absorption of autoantibodies by serum autoantigens; large numbers of plaque-forming cells (PFC) directed against mouse albumin and mouse transferrin were easily detected in the spleens of MRL/Mp-lpr/lpr, BXSB, and NZB mice. The secreted antibodies were relatively specific for the mouse proteins, since only limited cross-reactivity was seen with albumin and transferrins of other species in inhibition experiments. The production of these hidden antibodies could not be the result of diffuse polyclonal B cell activation, since the PFC to mouse transferrins and albumin were not always accompanied by comparable numbers of PFC against related albumins and transferrins. The results indicate that autoantibody production in murine lupus is a generalized phenomenon, not limited to the production of autoantibodies to nuclear or other cell-bound antibodies. However, the relative specificity of the autoantibodies for self-antigens indicates that diffuse polyclonal B cell activation cannot be the mechanism responsible, and argues that a selective mechanism, probably driven by antigen, accounts for production of autoantibodies in SLE.

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Prothrombin as Co-Factor of the Circulating Anticoagulant in Systemic Lupus Erythematosus?

Thrombosis and Haemostasis ◽

10.1055/s-0038-1654385 ◽

1959 ◽

Vol 03 (02) ◽

pp. 237-256 ◽

Cited By ~ 65

Author(s):

A Loeliger ◽

E. J. J Alsbach ◽

Keyword(s):

Systemic Lupus Erythematosus ◽

Lupus Erythematosus ◽

False Positive ◽

Immune Reaction ◽

Serum Proteins ◽

Normal Values ◽

Systemic Lupus ◽

Flocculation Test ◽

Tissue Thromboplastin ◽

Possible Cause

SummaryA 35-year old man with lupus erythematosus of the skin is demonstrated, who also shows signs of systemic L. E.: sometimes slightly increased ESR, varying thrombocytopenia, slightly prolonged coagulation and prothrombin time, positive cepnalin-cholesterol flocculation test, biologically false positive syphilis reactions and signs of a slightly increased haemolysis. Electrophoretic examination of the serum proteins presents practically normal values, certainly no hypergammaglobulinaemia. Analytical examination of coagulation reveals hypoprothrombinaemia and an anticoagulant most probably directed against thrombocyte factor 3, intrinsic thromboplastin and tissue thromboplastin. The anticoagulant seems to be only active in the presence of prothrombin. Prothrombin therefore, is considered a co-factor of the anticoagulant. The inactive anticoagulant is localized in the gamma globulins. The possible cause of the hypoprothrombinaemia (immune reaction?) and the data in the literature are discussed.

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Serum Complement, Rheumatoid Factor, and Other Serum Proteins in Rheumatoid Disease and Systemic Lupus Erythematosus

Annals of the Rheumatic Diseases ◽

10.1136/ard.18.3.215 ◽

1959 ◽

Vol 18 (3) ◽

pp. 215-224 ◽

Cited By ~ 32

Author(s):

H. A. Ellis ◽

D. Felix-Davies

Keyword(s):

Systemic Lupus Erythematosus ◽

Rheumatoid Factor ◽

Lupus Erythematosus ◽

Serum Proteins ◽

Serum Complement ◽

Rheumatoid Disease ◽

Systemic Lupus

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ROLE OF GAMMA GLOBULINS IN PATHOGENESIS OF RENAL LESIONS IN SYSTEMIC LUPUS ERYTHEMATOSUS AND CHRONIC MEMBRANOUS GLOMERULONEPHRITIS, WITH AN OBSERVATION ON THE LUPUS ERYTHEMATOSUS CELL REACTION

Journal of Experimental Medicine ◽

10.1084/jem.106.2.191 ◽

1957 ◽

Vol 106 (2) ◽

pp. 191-202 ◽

Cited By ~ 112

Author(s):

Robert C. Mellors ◽

Louis G. Ortega ◽

Halsted R. Holman

Keyword(s):

Systemic Lupus Erythematosus ◽

Lupus Erythematosus ◽

Serum Proteins ◽

Fluorescent Antibody ◽

Periodic Acid ◽

Membranous Glomerulonephritis ◽

Systemic Lupus ◽

Periodic Acid Schiff ◽

Renal Lesions ◽

Γ Globulins

Utilizing the fluorescent antibody method for the histologic demonstration of localized γ-globulins, we have made the following observations (in contradistinction to the lack of such findings in a variety of normal and pathologic, control kidneys). In systemic lupus erythematosus (a) γ-globulins were localized in the thickened capillary walls, the "wire-loop" lesions, and the so called "hyaline thrombi" in glomeruli; (b) these sites of localization of γ-globulins were correlated to a considerable degree with the pattern of accentuated eosinophilia of the glomeruli, as seen in hematoxylin-eosin sections, or with the pattern of PAS-positive areas in the glomeruli in sections stained with the periodic acid-Schiff reaction; (c) and γ-globulins were localized rarely in large cytoplasmic granules in tubular epithelium and occasionally in glomerular capsular crescents, tubular protein casts, and inflammatory cells, particularly in the cytoplasm of cells identified as immature and mature plasma cells. In nephrotic glomerulonephritis (a) γ-globulins were localized in the glomerular basement membrane and appertaining structures in chronic membranous glomerulonephritis; (b) γ-globulins were apparently localized in the altered mesangium in chronic lobular glomerulonephritis; and (c) in the tubular protein casts, presumably representing abnormal glomerular filtrates, γ-globulins were present in a lesser concentration and other serum proteins in a greater concentration than found in the glomeruli. In positive lupus erythematosus preparations the nuclei of leukocytes, while undergoing transformation and subsequent phagocytosis to form lupus erythematosus cells, were the sites of localization of γ-globulin (presumably the lupus erythematosus factor) whereas in control preparations no nuclear localization of γ-globulin occurred. These observations are discussed in relation to the pathogenesis of renal lesions in systemic lupus erythematosus, chronic membranous glomerulonephritis, and amyloidosis.

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Canine Systemic Lupus Erythematosus

Blood ◽

10.1182/blood.v25.2.143.143 ◽

1965 ◽

Vol 25 (2) ◽

pp. 143-160 ◽

Cited By ~ 84

Author(s):

ROBERT M. LEWIS ◽

ROBERT SCHWARTZ ◽

WILLIAM B. HENRY

Keyword(s):

Systemic Lupus Erythematosus ◽

Lupus Erythematosus ◽

Autoimmune Hemolytic Anemia ◽

Serum Proteins ◽

Antithyroid Antibody ◽

Systemic Lupus ◽

Thrombocytopenic Purpura ◽

Renal Lesions ◽

Naturally Occurring ◽

Immunologic Disease

Abstract A naturally occurring immunologic disease, characterized by autoimmune hemolytic anemia, idiopathic thrombocytopenic purpura and nephritis, is described in seven dogs. The disease primarily affected formed elements in the blood, glomeruli and blood vessels. Abnormal serum proteins, including the LE factor, rheumatoid factor and antithyroid antibody were found in affected dogs. Corticosteroids and splenectomy were effective in controlling the hematologic components of the disease, but apparently had no effect on the renal lesions. Recurrence was frequent and the prognosis was grave. Additional abnormalities, including malar eruption, intermittent lameness and alopecia were occasionally found as an integral part in the sequential involvement of several tissues during the course of the disease.

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Organized Intraglomerular Deposits in NZB Mouse Disease

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100066772 ◽

1971 ◽

Vol 29 ◽

pp. 544-545

Author(s):

Francis R. Comerford ◽

Alan S. Cohen

Keyword(s):

Systemic Lupus Erythematosus ◽

Lupus Erythematosus ◽

Antinuclear Antibodies ◽

Human Systemic Lupus Erythematosus ◽

Systemic Lupus ◽

Glomerular Lesion ◽

Ultrastructural Studies ◽

Dense Deposits ◽

Experimental Nephritis ◽

Glomerular Lesions

Mice of the inbred NZB strain develop a spontaneous disease characterized by autoimmune hemolytic anemia, positive lupus erythematosus cell tests and antinuclear antibodies and nephritis. This disease is analogous to human systemic lupus erythematosus. In ultrastructural studies of the glomerular lesion in NZB mice, intraglomerular dense deposits in mesangial, subepithelial and subendothelial locations were described. In common with the findings in many examples of human and experimental nephritis, including many cases of human lupus nephritis, these deposits were amorphous or slightly granular in appearance with no definable substructure.We have recently observed structured deposits in the glomeruli of NZB mice. They were uncommon and were found in older animals with severe glomerular lesions by morphologic criteria. They were seen most commonly as extracellular elements in subendothelial and mesangial regions. The deposits ranged up to 3 microns in greatest dimension and were often adjacent to deposits of lipid-like round particles of 30 to 250 millimicrons in diameter and with amorphous dense deposits.

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