Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Properdin”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,693 records · Page 94Linked to original sources
PubMed1978

IgA nephropathy: clinicopathology and immunopathology.

In a total of 283 biopsies, 100 (35%) were found to be IgA nephropathy. The incidence reached 40% among primary glomerulonephropathies. On the basis of histopathologic changes in glomeruli, these biopsies were classified into 3 groups. The criteria employed correlated well with clinical, laboratory and immunofluorescent findings. Immune complex pathogenesis was discussed in relation to our findings.

Adolescent↗
PubMed1991

Inherited complement deficiency states and disease.

Studies of inherited complement deficiency states in disease have provided a set of apparent biological facts relating to the protective importance of an intact complement system. While some of the findings seem to confirm what may have been expected on the basis of in vitro studies, other observations constitute a challenge to further investigation. In this presentation, basic findings with regard to deficiency of circulating complement proteins are briefly summarized, and some difficulties and issues of possible interest pointed out.

Bacterial Infections↗
PubMedDate not supplied

Complement receptors and regulatory proteins in human atherosclerotic lesions.

Complement activation in human atherosclerotic lesions is indicated by the presence of C5b-9 terminal complexes. By using monoclonal antibodies to the complement C3b receptor (CR1) and the iC3b receptor (CR3), it was observed that approximately 20% of the cells in complicated human carotid lesions express CR1 and CR3 antigens. One to five percent of complement receptor-positive cells stained for smooth muscle cell-specific myosin, and the remainder were determined to be predominantly macrophages, based on their reactivity to anti-LeuM3 (CD14) monoclonal antibody. No C3dg receptor (CR2)-positive cells were observed in any of the eight lesions examined. The complement regulatory glycoprotein decay accelerating factor (DAF) was widely distributed extracellularly, in addition to being present on 20% to 60% of the total cell population. Factor H, a plasma protein that regulates alternative pathway C3 convertase formation, was observed extracellularly in 70% of the lesions examined. C1 inhibitor was present in a few plaque specimens, was relatively sparse, and appeared largely cell associated. Terminal C5b-9 complement complexes were pervasive in all lesions. Both the complement regulatory proteins and the activation products were limited to the area of lesion involvement and were absent from normal arterial wall. The results demonstrate that molecules involved in complement regulation and complement ligand binding are present in atherosclerotic lesions, where they may function to modulate the activities of complement.

Arteriosclerosis↗
PubMed1973

C2 deficiency. Development of lupus erythematosus.

The study of serum from a patient with C2 deficiency is described. The patient had an episode of pneumococcal meningitis at 5 mo of age with seizures and transient hemiparesis and apparent purpuric skin lesions. He was first admitted to the University of Minnesota Hospitals at 10 yr of age following the discovery of proteinuria accidentally by his mother. Since then he has been admitted repeatedly to this hospital with numerous clinical findings including arthralgia, recurrent abdominal pain, proteinuria, membranous nephropathy, malar butterfly rash, seizures, personality aberrations, and recurrent fever. In June 1971, the patient developed positive DNA and DNP antibodies and positive LE cells. When the C profile was studied before and after recognition of lupus, C1q, C1s, and C4 dropped. C3 levels were elevated as were C5, C6, and C7, C3 proactivator had been reduced in the patient even before he developed lupus. Also because of a traumatic renal biopsy leading to a perirenal hematoma, he required surgery and a blood transfusion. 1 h after blood transfusion, a C2 titer of 23 hemolytic units was detected. Almost immediately levels of C3, C5, C6, and C7 dropped, C8 and C9 remained elevated. The addition of C2 from normal blood permitted dramatic activation of C3. These findings support the view that the rare deficiency in production of C2 predisposes to serious susceptibility to infection, vascular and mesenchymal disease as well as to renal disease and a lupus syndrome.

Antibodies↗
PubMed1974

Metabolic studies of the third component of complement and the glycine-rich beta glycoprotein in patients with hypocomplementemia.

Metabolic studies using radioiodine-labeled third component of complement (C3) and the glycine-rich beta glycoprotein (GBG), a major component of the C3b-feedback pathway, were undertaken in normal subjects, in 22 patients with evidence of complement activation, and in 11 patients with various renal diseases without evidence of complement activation. In seven normal subjects GBG was found to be a rapidly metabolized protein with catabolic rates ranging from 1.7% to 2.2% of the plasma pool/h, synthesis rates from 0.14 to 0.21 mg/kg per h. and extravascular/intravascular distribution ratios from 0.81 to 1.31. In patients with reduced plasma C3, both increased C3 fractional catabolic rates and reduced C3 synthesis rates were observed, and in some patients there was evidence of increased extravascular distribution of the protein. GBG catabolism was usually increased when there was evidence of C3 activation, presumably reflecting activation of the C3b-feedback; but GBG turnover was normal or only slightly accelerated in some patients with accelerated C3 catabolism and profound hypocomplementemia, suggesting that reduced C3 synthesis had limited activation of the C3b-feedback.

Complement Inactivator Proteins↗
PubMed1984

Reduction of phagocyte adherence by nephritic sera: relation to complement activation.

Phagocytes isolated from either normal donors or from patients with poststreptococcal (P-SGN), lupus erythematosus (SLE-GN), or membranoproliferative (MPGN) glomerulonephritis showed normal adherence to glass (PAg) after incubation in normal human serum (NHS), but was reduced after incubation in patient serum. Low PAg was the consequence of incubation of normal phagocytes with the earliest available sera from all 22 P-SGN patients, 28 of 37 SLE-GN patients, 19 of 25 patients with MPGN type I, all 10 with types II and III, and all 5 with nephritis associated with chronic bacteremia. Low C3 and decreased PAg were related by regression analysis in sera from patients with P-SGN (P less than 0.001), SLE-GN (P less than 0.005), and MPGN (P less than 0.001) type I. In patients with P-SGN and one patient with nephritis associated with chronic bacteremia, complement levels and PAg returned to normal in parallel with clinical improvement. In vitro, PAg was reduced by NHS treated with either zymosan or bovine serum albumin (BSA)-anti-BSA complexes but neither BSA-anti-BSA complexes or zymosan, previously incubated in NHS, reduced PAg. PAg was normal in serum deficient in C4 or C5 unless treated with zymosan.

Adult↗
PubMedDate not supplied

Renal manifestation of pustulosis palmaris et plantaris.

Diffuse proliferative glomerulonephritis without IgA deposits (DPGN) in patients with pustulosis palmaris et plantaris (PPP) is described. This association has not been previously reported. Although PPP was resolved transiently after tonsillectomy, it was worsened coincidently at the time of exacerbation of DPGN. Improvement of proteinuria and PPP was observed after antiplatelet therapy. It was suggested that the renal manifestation and the development of PPP were associated.

Blood Platelets↗
PubMed1980

Different serum requirements for opsonization of two serologically identical strains of Pseudomonas aeruginosa.

Two strains of serotype 2 Pseudomonas aeruginosa and one species of E. coli were compared regarding their opsonic requirements using human sera and polymorphonuclear leukocytes. None of the three organisms tested activated exclusively one complement pathway. Both strains of Pseudomonas had an absolute requirement for antibody for opsonization, but differed in complement requirements. The studies described herein showed significant differences in the mechanism of opsonization of the two strains of Pseudomonas.

Binding Sites, Antibody↗