Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Complement C1q”

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 469 records · Page 26Linked to original sources
PubMed1985

[Immunologic laboratory tests in acquired immunodeficiency syndrome (AIDS) and suspected AIDS].

Since AIDS-specific laboratory tests are not yet commercially available, laboratory diagnoses of AIDS or of the AIDS-related complex (ARC) are based on "surrogate markers". While single tests are of limited diagnostic value, test combinations are of greater help. However, these tests should be applied restrictively and stepwise. The following parameters were analyzed in respect of their diagnostic and differential-diagnostic value: absolute number of lymphocytes, delayed type hypersensitivity skin tests to seven recall antigens, beta-2-microglobulin, serum-neopterin, C-reactive protein, complement factor B, circulating immune complexes, immunoglobulins, hepatitis B markers, and the ratio of T helper to T suppressor cells. 14 AIDS patients, 11 ARC patients, 23 healthy homosexuals, 6 iv drug users, 6 hemophiliacs and 35 patients with various other disorders were investigated. To analyse the value of a given test or of test combinations in the diagnosis of AIDS and ARC, a discrimination index was introduced and defined as the difference between the percentage of pathological values in one patient group compared to the percentage of pathological values in the other group. A discrimination index of 100 means that a given test is pathologic in all members of one group and negative in all members of the other group. A discrimination index of 60 may mean 80% of pathological values in one group versus 20% in the other. To distinguish AIDS patients from ARC patients the test combination yielding the highest mean discrimination index included serum neopterin, complement factor B and C-reactive protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

[Synovial level of interleukin 1 and C3a in chronic polyarthritis, psoriatic arthritis and activated arthritis].

Concentrations of interleukin-1 (IL-1), C3a des Arg and immune complexes (IC) were investigated in knee effusions of patients with rheumatoid arthritis (RA; n = 36), psoriatic arthritis (Ps.A., n = 19) and osteoarthritis (n = 7). Maximal concentrations of IC and C3a des Arg were found in RA patients, high IL-1-activities could be demonstrated in patients with Ps.A. and seropositive RA. We found significant correlations between IL-1 and C3a des Arg, IL-1 and IC and C3a des Arg, and IC in Ps.A. patients, but not in RA or osteoarthritis patients. The role of IL-1 in the chronic inflammatory response and joint destruction in inflammatory joint diseases is discussed.

Adult↗
PubMed1986

[Inhibition of the binding and activation of the first component of human complement. The effect of synthetic peptides, immunoglobulin fragments and various proteins].

A study has been carried out on the inhibition of the subcomponent Clq binding to sensitized sheep erythrocytes (EA) by the following synthetic peptides mimicking the structure of a putative complement binding site of immunoglobulin G: Boc-Trp-Tyr, Boc-Tyr-Trp, Trp-Tyr, Boc-Trp-Phe, Boc-D-Trp-D-Tyr, Boc-D-Tyr-D-Trp, Boc-Leu-Leu, Ac-Phe-Tyr, and commercial Thr-Lys-Pro-Arg (tuftsin). Boc-Trp-Tyr was found to be the most potent inhibitor of Clq binding to EA (Ki 2.86 X 10(-4) M), tuftsin ranking second with Ki 6 X 10(-4) M. The D,D-dipeptides failed to inhibit the Clq binding at the investigated concentrations. Insoluble Z-Trp-Tyr-OMe activated a classical pathway of complement system, as monitored by consumption of C4, C2 and C3 components. Synthetic octapeptide Boc-Glu-Val-Asp-Leu-Leu-Lys-Asp-Glu-OMe (corresponding to the sequence 36-43 of beta 2-microglobulin) inhibited the Clq binding with Ki 4.7 X 10(-4) M, which gave grounds for localizing the complement binding site in beta 2-microglobulin. The finding in the Clq structure of the peptide sequence homologous to than of the pepsin active site, as well as the close similarity in the specificity of these proteins towards hydrophobic amino acid residues justified the assumption on the same structural bases of their specificity. The results of the present study, along with the literature data, underlie the hypothesis on the involvement in the complement binding of the following IgG residues: Trp277, Tyr278, Lys320, Lys322, Glu318 and Lys290. The enlisted residues are closely located in the three-dimensional structure of the CH2 domain of IgG. Lysozyme and lactalbumin having the sequences homologous to Trp277-Tyr278 of IgG inhibited Clq binding to EA with Ki 3 and 1.5 microM respectively.

Amino Acid Sequence↗
PubMed1986

Changes of serum complement concentrations in tumour patients prior and after radiotherapy.

Peripheral blood concentrations of leucocytes, platelets and complement factors Clq, C3c, C3d, C4 and C5 were examined in 30 patients suffering from malignant tumours prior and after radiotherapy. In general, a decrease of blood cell concentrations as well as serum complement levels was noted using regression analysis. Two groups were formed: patients with (group I) and without (group II) foregoing tumour surgery. A positive correlation was found for all complement factors prior therapy in group I, whereas only some complement components did correlate in group II. The results in group I are in agreement with complements classical pathway activation. We conclude that the alternative pathways influence is responsible for the different results in group II.

Combined Modality Therapy↗
PubMed1987

Dense deposit disease: its possible pathogenesis suggested by an observation of a patient.

A girl, aged 8, was admitted to a hospital in a state of nephrotic syndrome of one year's duration. The renal biopsy showed mesangial and endocapillary proliferations with lobulation. Dense deposit was not demonstrated by electron microscopy, but lamellation of the lamina densa was found in most of the capillary loops. Her condition was improved by steroid treatment in a few months, but moderate proteinuria persisted. Five and half years later, follow-up biopsy showed typical pathological features of dense deposit disease. It is suggested that the lamellation of the lamina densa in the first biopsy could be related to the dense alteration of glomerular basement membrane in the second biopsy.

Basement Membrane↗
PubMed1985

[Recurrent hemolytic-uremic syndrome with positive immunofluorescence].

The hemolytic uremic syndrome is a disease of infancy, its major clinical manifestations include reversible thrombocytopenia, hemolytic anemia, and renal failure. Although a great number of patients with HUS have been published, relapses as well as positive immunofluorescence studies are rare findings. In our patient the disease began at age of 7 years and recovered completely. At 10 1/2 years a relapse occurred and despite therapy the patient died two months later. Renal biopsy showed severe arterial and glomerular changes with remarkable similarity to the histological findings in thrombotic thrombocytopenic purpura, which could be explained as secondary hypertensive damage, and dense granular deposition of fibrinogen, IgG, IgA, C3, and Clq along the capillary loops of the glomerulus and throughout the wall of the renal arteries. The clinical data, histological findings, and the particularities of our patient with this special course of HUS are discussed.

Child↗
PubMed1985

[Current diagnostic possibilities in hereditary angioedema and acquired angioedema].

Amidolytic assays for the determination of C1 esterase inhibitor have been proposed some years ago; however, the substrates employed lacked sensitivity. The recent development of a C1 esterase-sensitive substrate (N-alpha-methoxycarbonyl-l-lysyl(epsilon-CBO)-glycyl-arginyl-4-nit roanilide) provides a method that can be routinely used. Any interferences with other plasma proteases could not be observed. Normal range was ascertained to be 1.48 +/- 0.23 kU/l; within-run precision revealed C.V.'s of 1.74% (for the normal range) and 7.3% (for the pathological range). This method can be considered most suitable for functional determination of C1 esterase inhibitor and is superior to the determination of antikallikrein activity. To point out to the diagnostic relevance of a functional C1 esterase inhibitor assay some examples are illustrated.

Angioedema↗
PubMed1983

Primary macroglobulinemia presenting as multiple ulcers of the legs.

Multiple ulcers developed on the lower legs of a 67-year-old man suffering from macroglobulinemia. Histological and direct immunofluorescence studies on biopsy specimens taken from the lesions revealed dilation of capillaries, deposition of large quantities of IgM in the vessels, and deposition of C3 in the vessel walls. A marked increase in blood Clq binding immune complexes was also noted. These findings suggest immune complex-induced ulceration. The fact that IgM-type cryoglobulins were positive implies that cryoglobulins derived from macroglobulins may play an important causative role in ulceration.

Aged↗
PubMed1984

Hepatitis B surface antigen containing immune complexes occur in seronegative hepatocellular carcinoma patients.

IgG, IgM and hepatitis B surface antigen (HBsAg) containing immune complexes (IC) were detected by the Clq and conglutinin solid phase assays in both HBsAg+ and HBsAg- groups of patients with primary hepatocellular carcinoma (HCC). No differences were observed between the two patient groups either in the levels of antigen non-specific and HBsAg specific complexes or in the immunoglobulin isotype in the complexes. The results show that HBsAg can occur in an IC form in the sera of patients classified as HBsAg- by sensitive commercial assays and provides evidence of a further association of hepatitis B virus (HBV) and HCC in antigen negative patients. Furthermore, the HBsAg IC in HCC patients differ from those in other HBV infected subjects in that they are preferentially detected by the Clq assay.

Antigen-Antibody Complex↗
PubMed1982

[Hereditary complement deficiencies].

Complement deficiencies of all nine C-components have been observed. Hereditary defects of early components of the classical pathway - C1, C4, C2 - are often associated with diseases of the immuncomplex-type especially with systemic lupus erythematosus, dermatomysitis, vasculitis and nephritis. Deficiencies of C3 and C3b inactivator are linked to severe and recurrent bacterial infections. Patients with hereditary defects of the so-called late components, C5-C9, show increased susceptibility to recurrent disseminated infections by neisseria gonorrhoeae and meningitidis. The most frequent of the defects of the complement system is the hereditary deficiency of C1-inactivator which is associated with hereditary angioneurotic edema. In this paper the C-defects and their genetics are described and possible pathomechanisms are discussed.

Complement Activating Enzymes↗