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PubMed2001

Thrombangitis obliterans: leucocyte subpopulations and circulating immune complexes.

BACKGROUND: The etiology of thrombangitis obliterans is still unclear. Although cellular infiltration of the vessel wall is known, no studies on peripheral blood mononuclear cells are reported. Therefore, we assessed leucocyte subpopulations and circulating immune complexes in patients with thrombangitis obliterans and a control group of normal people. PATIENTS AND METHODS: 31 patients (40 +/- 2 years, 24 male, 7 female) with thrombangitis obliterans were included, based on the following criteria: age of manifestation, acral ischemia in legs and arms, previous thrombophlebitis or phlebitis saltans. Manifestation of atherosclerosis or other vasculitic manifestations were excluded. Leucocyte subpopulations, levels of C-reactive protein (CRP) and circulating immune complexes (CIC) were investigated. An age-matched control group (n = 25) was recruited from voluntary blood donors. RESULTS: Leucocyte counts in the thrombagitis group (mean +/- SD: 10,839 +/- 782/nl) were significantly different from the control group (6205 +/- 414/nl, p < 0.0001). The same was true for absolute counts of granulocytes, monocytes and lymphocytes. The results were independent from CRP, which was elevated only in 6 patients. Relative counts of naive helper T-cells were significantly lower in the patient group. HLA-DR expression on B-cells was lower on the patients' lymphocytes. The concentrations of IgA, IgG and IgM in CIC were higher in the thrombangitis patients compared to the control group. C1q-binding capacity and phosphatidylserine antibodies showed no differences. CONCLUSIONS: Patients suffering from thrombangitis obliterans show alterations of leucocyte counts and their subpopulations as well as alterations of the humoral (IgCIC) immune system.

Adult↗
PubMed2004

Spinal cord involvement in the nonhuman primate model of Lyme disease.

Lyme borreliosis is a multisystemic disease caused by infection with various genospecies of the spirochete Borrelia burgdorferi. The organs most often affected are the skin, joints, the heart, and the central and peripheral nervous systems. Multiple neurological complications can occur, including aseptic meningitis, encephalopathy, facial nerve palsy, radiculitis, myelitis, and peripheral neuropathy. To investigate spinal cord involvement in the nonhuman primate (NHP) model of Lyme borreliosis, we inoculated 25 adult Macaca mulatta with B. burgdorferi sensu strictu strains N40 by needle (N=9) or by tick (N=4) or 297 by needle (N=2), or with B. burgdorferi genospecies garinii strains Pbi (N=4), 793 (N=2), or Pli (N=4) by needle. Immunosuppression either transiently (TISP) or permanently (IS) was used to facilitate establishment of infection. Tissues and fluids were collected at necropsy 7-24 weeks later. Hematoxylin and eosin staining was used to study inflammation, and immunohistochemistry and digital image analysis to measure inflammation and localize spirochetes. The spirochetal load and C1q expression were measured by TaqMan RT-PCR. The results showed meningoradiculitis developed in only one of the 25 NHP's examined, TISP NHP 321 inoculated with B. garinii strain Pbi. Inflammation was localized to nerve roots, dorsal root ganglia, and leptomeninges but rarely to the spinal cord parenchyma itself. T cells and plasma cells were the predominant inflammatory cells. Significantly increased amounts of IgG, IgM, and C1q were found in inflamed spinal cord. Taqman RT-PCR found spirochetes in the spinal cord only in IS-NHP's, mostly in nerve roots and ganglia rather than in the cord parenchyma. C1q mRNA expression was significantly increased in inflamed spinal cord. This is the first comprehensive study of spinal cord involvement in Lyme borreliosis.

Animals↗
PubMed2004

Interaction of C1q with the receptor calreticulin requires a conformational change in C1q.

The interaction between C1q and the chaperone calreticulin was studied under various conditions. When both proteins were present in equal amounts in solution, no interaction could be demonstrated. However, C1q immobilized on a hydrophobic surface, exposed to heat-treatment or bound to immunoglobulins (Igs) showed a strong, rapid and specific binding of calreticulin. The interaction appeared to be a two-step process, and the initial phase of interaction was sensitive to high concentrations of salt but not to a physiological salt concentration. The following strong binding was insensitive to salt and extremes of pH but sensitive to strongly denaturing agents (urea and guanidine). The sensitivity to salt during the initial phase of interaction was practically identical to that observed when calreticulin was bound to type V collagen. Binding between C1q and calreticulin could be inhibited by serum amyloid P component and by proteinase K-digested ovalbumin, and the binding of calreticulin to proteinase K-digested ovalbumin was shown to be inhibited by C1q. The data indicate that C1q binds stably to the peptide-binding site of calreticulin and that the initial binding of calreticulin to C1q involves the collagen-like domain of the C1q molecule. In conclusion, our results suggest calreticulin as a potential receptor for an altered conformation of C1q as occurs during binding to Igs. Thus, the chaperone and protein-scavenging function of calreticulin may extend from the endoplasmic reticulum to the topologically equivalent cell surface, where it may contribute to the elimination of immune complexes and apoptotic cells.

Animals↗
PubMed2006

Reduced expression of C1q-mRNA in monocytes from patients with systemic lupus erythematosus.

Inherited C1q deficiency is associated strongly with the development of systemic lupus erythematosus (SLE). The aim of our study was to evaluate the ability of monocytes from SLE patients without inherited C1q deficiency to up-regulate C1q-mRNA upon stimulation. Furthermore, we wanted to elucidate the physiological stimulus for up-regulation of C1q-mRNA. Peripheral blood mononuclear cell (PBMC)-derived monocytes from 10 SLE patients, 10 patients with rheumatoid arthritis (RA) and 10 healthy controls (HC) were stimulated with dexamethasone (DXM), interferon-gamma or both. Additionally, purified monocytes from HC were stimulated with interleukin (IL)-10. C1q-mRNA expression was measured by quantitative reverse transcription-polymerase chain reaction (RT-PCR). C1q protein was detected using the standard alkaline phosphatase/anti-alkaline phosphatase (APAAP) technique. SLE monocytes were significantly less able to up-regulate C1q-mRNA when compared to RA or HC. IL-10 was identified as an important stimulus for C1q synthesis. In SLE patients there is a significant functional impairment of monocytes to synthesize C1q upon stimulation. As C1q is linked to the process of recognition and removal of apoptotic cells, this relative C1q deficiency is likely to contribute to the reduced phagocytosis of apoptotic material observed in SLE and thereby might be a central pathogenetic factor.

Adult↗
PubMed1983

Virus-induced immune complex disease: genetic control of C1q binding complexes in the circulation of mice persistently infected with lymphocytic choriomeningitis virus.

Virus-antibody immune complex formation, deposition, and disease is a common manifestation in most mice persistently infected with lymphocytic choriomeningitis virus (LCMV). Although mice of several strains persistently infected with LCMV mount continuous anti-LCMV immune responses to the three virion structural polypeptides, the amount of antibody(s) made varies among strains. The formation of antibody to LCMV correlates with the detection of C1q binding materials (immune complexes) in the circulation; however, there is no correlation between the total amount of IgG and the C1q binding material. SWR/J mice (H2qq) are high responders (high levels of anti-LCMV antibodies, high C1q binding responses), whereas BALB/W mice (H-2dd) are low responders (low levels of anti-LCMV antibodies, low C1q binding responses). Sera from 37 SWR/J mice, 12 wk of age, bound 55.1% of offered 125I C1q compared to 8.4% for 37 age and sex-matched BALB/W mice. SWR/J mice made approximately 60-fold more antibody to LCMV than did BALB/W mice. To define the genetic factors involved, we used the C1q binding assay, high responder and low responder mice, their hybrid offspring, backcrosses of the hybrids to both high and low responder parents, and selected recombinant inbred mouse strains. From studies with BALB/W mice persistently infected with LCMV, we defined low C1q responder mice as those having binding activity of 18.4% or less (BALB/W mean C1q binding value + 2 SD). By using this criteria for 12-wk-old mice, 55/57 (96%) of SWR/J, 27/37 (73%) of F1(SxB or BxS), 13/21 (62%) of qq or 11/20 (55%) qd from F1 x SWR/J, and 6/13 (45%) qd from F1 x BALB/W were high C1q responders. In contrast, none of the 17 dd mice from the F1 x BALB/W cross were high responders. Thus, F1 hybrid mice are high responders (dominant) and data from backcrossing F1 hybrids to either high or low responder parents suggested the complexes associated with C1q binding was controlled by gene(s) in the H-2 complex. Support for the role of Ir gene(s) was provided by experiments showing LCMV persistently infected BALB/kae (H-2 KkIkDk) and recombinant inbred strains B10.A (KkIkDd) and A.TL (KsIkDd) were high C1q responders, whereas B10.A(5R) (KbIbDd) and BALB/cby (KdIdDd) were not. The wide scatter in C1q binding levels observed among C1q high responder mice and the production of C1q binding levels in F1 mice that are intermediate between high and low responder strains suggested that, in addition to H-2-linked genes, other non-H-2-linked genes also play a role in this response. The amount of C1q binding complexes in LCMV persistently infected mouse strains and their crosses was unrelated to the amounts of infectious virus carried in their sera. Despite the low C1q binding by sera of H-2dd mice that originated from mating F1 hybrid (qd) x BALB/WEHI (dd), these mice carried equivalent amounts of infectious virus as their qd littermates or qd and qq mice originated from F1 x SWR/J mice.

Animals↗
PubMedDate not supplied

Use of high-dose intravenous immunoglobulin in systemic lupus erythematosus: report of three cases.

Three patients with life-threatening manifestations of systemic lupus erythematosus (SLE), unresponsive to conventional high-dose corticosteroid and/or immunosuppressive therapy were treated with intravenous polyspecific IgG (IVIG). Following IVIG infusion, lupus encephalitis in the first patient quickly resolved and the impressive improvement of the clinical status was associated with a transient increase in C1q-binding activity. The daily infusion of IgG had to be suspended after three days in the second patient with encephalitis and nephritis, because the renal function rapidly deteriorated; subsequently, six plasma exchanges led to an almost complete recovery. Finally, leukocyte and platelet counts increased and remained within normal range following IgG therapy in the third patient having SLE-associated leuko- and thrombocytopenia. In all three patients a decrease in anti-DNA antibody levels and an increase in total complement hemolytic activity were detected after therapy.

Adolescent↗
PubMed2006

Modulation of the effector functions of a human IgG1 through engineering of its hinge region.

We report here the engineering of a humanized anti-human EphA2 mAb (mAb 12G3H11) in an effort to explore the relationship between the hinge of a human IgG1 and its effector functions. mAb 12G3H11, used here as a model, is directed against the human receptor tyrosine kinase EphA2, which is an actively investigated target for cancer therapy due to its up-regulation in many cancer cells. Various rational modifications were introduced into the hinge region of mAb 12G3H11. These mutations were predicted to modulate the hinge's length, flexibility, and/or biochemical properties. We show that the upper and middle hinge both play important, although functionally distinct roles. In particular, middle hinge modifications predicted to decrease its rigidity or length as well as eliminating either one of its two cysteine residues had a strong negative impact on C1q binding and complement-dependent cytotoxicity. Disruption of covalent bonds between both H chains may account in part for these effects. We also describe middle hinge mutants with a significantly decreased ability to bind FcgammaRIIIA and trigger Ab-dependent cell-mediated cytotoxicity. Conversely, we also generated upper hinge mutants exhibiting an increase in C1q binding and complement-dependent cytotoxicity activity. Therefore, this approach represents a novel strategy to fine-tune the biological activity of a given human IgG1. We also define, for the first time in such a systematic fashion, the relationship between various characteristics of the middle and upper hinge and the corresponding effector functions.

Amino Acid Sequence↗
PubMed2002

Cooperation of C1q receptors and integrins in C1q-mediated endothelial cell adhesion and spreading.

The interaction of C1q with endothelial cells elicits a multiplicity of biologic responses. Although these responses are presumed to be mediated by the interaction of C1q with endothelial cell surface proteins, the identity of the participants is not known. In this study we examined the roles of two C1q binding proteins, cC1q-R/calreticulin and gC1q-R/p33, in C1q-mediated adhesion and spreading of human dermal microvascular endothelial cells (HDMVEC). When HDMVEC were cultured in microtiter plate wells coated with concentrations of C1q ranging from 0 to 50 microg/ml, a specific and dose-dependent adhesion and spreading was observed. The extent of adhesion and spreading was similar to the adhesion seen on collagen-coated wells. Spreading (68 +/- 12%) and to a moderate extent adhesion (47 +/- 9%) were inhibited by anti-gC1q-R mAb 60.11. Similar effects were noted with polyclonal anti-cC1q-R but not with control nonimmune IgG. The two Abs had a slight additive effect (75 +/- 13% inhibition) when mixed together in the proportion of 100 microg/ml anti-gC1q-R and 30 microg/ml anti-cC1q-R. More importantly, a 100% inhibition of spreading, but not adhesion, to C1q-coated wells was observed when HDMVEC were cultured in the presence of 30 microM of the peptide GRRGDSP but not GRRGESP. Furthermore, while anti-beta(1) integrin Ab blocked both adhesion and spreading, anti-alpha(5) integrin blocked only spreading and not adhesion. Ag capture ELISA of endothelial cell membrane proteins using polyclonal anti-gC1q-R showed the presence of not only beta(1) and alpha(5) integrins but also CD44. Taken together these results suggest that endothelial cell adhesion and spreading require the cooperation of both C1qRs and beta(1) integrins and possibly other membrane-spanning molecules.

Antibodies↗
PubMed1996

Human C1q induces eosinophil migration.

Eosinophils (Eo) play a significant role in allergic inflammation and the host's immunity to parasitic infections. Although the presence of C1q-binding cell surface molecule(s) (C1q-R) on Eo had been previously implicated by the ability of C1q to augment IgG-dependent, Eo-mediated killing of schistosomula, little is known about the structure or the function of this receptor. The present studies were therefore undertaken to immunochemically demonstrate and to examine the biology of Eo C1q-R. Eo were purified to homogeneity (>90%) and viability (>98%) from hypereosinophilic donors by Percoll density gradient. Western blot analysis using antibodies to cC1q-R and gC1q-R showed distinct bands corresponding to cC1q-R (60 kDa) and gC1q-R (33 kDa) when immunoblotted with their respective antibodies. The Eo C1q-R was tested for its ability to induce chemokinesis and/or chemotaxis as assessed by the modified Boyden microchamber assay utilizing 5-micrometer-pore polycarbonate membranes and using C1q, cC1q, or gC1q (10 micrograms/ml) as agonists. The known chemotactic factors C5a and RANTES (10(-8)M) were used as positive controls. The results showed that at this concentration, cC1q was most efficient in its ability to induce Eo migration (20 +/- SEM 12, n = 4) followed by C1q (107 +/- SEM 7, n=7) and gC1q (77 +/- SEM 10, n = 10). When checkerboard analysis was performed, the data indicated that the observed phenomenon was likely to be due largely to chemokinesis. As expected, C5a (145 +/- SEM 15, n = 7) and RANTES (145 +/- SEM 43, n = 7) were both chemotactic. Furthermore, incubation of Eo with 50 micrograms of either C1q, gC1q, or cC1q (1 hr, 37 degrees C) did not cause release of eosinophil cationic protein as measured by RIA, nor did it enhance the expression of CD11b or CD29 as assessed by FACS analysis. The data presented in this paper show that Eo express both cC1q-R and gC1q-R and may participate in Eo function by providing a primary signal for locomotion.

Blood Proteins↗
PubMed2006

Complement component C3 mediates inflammatory injury following focal cerebral ischemia.

The complement cascade has been implicated in ischemia/reperfusion injury, and recent studies have shown that complement inhibition is a promising treatment option for acute stroke. The development of clinically useful therapies has been hindered, however, by insufficient understanding of which complement subcomponents contribute to post-ischemic injury. To address this issue, we subjected mice deficient in selected complement proteins (C1q, C3, C5) to transient focal cerebral ischemia. Of the strains investigated, only C3-/- mice were protected, as demonstrated by 34% reductions in both infarct volume (P<0.01) and neurological deficit score (P<0.05). C3-deficient mice also manifested decreased granulocyte infiltration (P<0.02) and reduced oxidative stress (P<0.05). Finally, administration of a C3a-receptor antagonist resulted in commensurate neurological improvement and stroke volume reduction (P<0.05). Together, these results establish C3 activation as the key constituent in complement-related inflammatory tissue injury following stroke and suggest a C3a anaphylatoxin-mediated mechanism.

Animals↗
PubMed2001

C1q and mannose binding lectin engagement of cell surface calreticulin and CD91 initiates macropinocytosis and uptake of apoptotic cells.

Removal of apoptotic cells is essential for maintenance of tissue homeostasis, organogenesis, remodeling, development, and maintenance of the immune system, protection against neoplasia, and resolution of inflammation. The mechanisms of this removal involve recognition of the apoptotic cell surface and initiation of phagocytic uptake into a variety of cell types. Here we provide evidence that C1q and mannose binding lectin (MBL), a member of the collectin family of proteins, bind to apoptotic cells and stimulate ingestion of these by ligation on the phagocyte surface of the multifunctional protein, calreticulin (also known as the cC1qR), which in turn is bound to the endocytic receptor protein CD91, also known as the alpha-2-macroglobulin receptor. Use of these proteins provides another example of apoptotic cell clearance mediated by pattern recognition molecules of the innate immune system. Ingestion of the apoptotic cells through calreticulin/CD91 stimulation is further shown to involve the process of macropinocytosis, implicated as a primitive and relatively nonselective uptake mechanism for C1q- and MBL-enhanced engulfment of whole, intact apoptotic cells, as well as cell debris and foreign organisms to which these molecules may bind.

Apoptosis↗
PubMed2000

Structural changes in porcine bioprosthetic valves of a left ventricular assist system in human patients.

BACKGROUND AND AIM OF THE STUDY: Porcine, specially manufactured bioprosthetic valves regulate blood flow from the left ventricle to pump sac (inflow valve) and from the pump to the aorta (outflow valve) in a wearable, electrically powered left ventricular support system (LVAS, Novacor). The increased need for long-term circulatory assistance requires information on the evolution of these valves when exposed to specific hemodynamic conditions and inflammatory reactions in the device. The study aim was to examine structural changes in valves from explanted LVASs. METHODS: Thirteen patients (11 males, two females; mean age 42 years (range: 17-64 years) were supported for a mean of 285 days (range: 37-1,293 days) with LVAS. Histologic sections from explanted inflow and outflow valves were studied immunohistochemically using peroxidase-labeled antibodies and avidin-biotinylated peroxidase complex for detection. RESULTS: In the macroscopically normal inflow valves (11/13), the outflow surface (facing the pump) was covered with a discontinuous deposit of fibrin, macrophages and granulocyte elastase. Fibrinogen, IgG, complement proteins C1q and C3 had infiltrated the extracellular matrix (ECM) between 37 and 1,293 days. The crevices were enlarged during circulatory support, and fibrinogen/fibrin insudations were detected in the spongiosa. The collagen layers in the fibrosa were disrupted after 293 days, and eroded on the inflow surface in the ventricularis after 1,293 days. In a deteriorated valve from a patient with endocarditis, Gram-positive bacteria and metalloproteinases were concentrated in the ECM. In the macroscopically normal (11/13) outflow valves, fibrin and complement proteins had penetrated the ECM from the inflow side (facing the pump), while macrophages and granulocytes were localized mainly on the outflow surface. IgG and complement proteins were detected on and beneath the cusp surface up to 200 days and covered the disrupted ECM as implant time progressed. CONCLUSIONS: Structural changes appear to progress more rapidly in the inflow than in the outflow of bioprosthetic valves. This difference indicates that the effects of biological factors are modulated by mechanical stress.

Adolescent↗
PubMed2004

Cooperation between C1q and DNase I in the clearance of necrotic cell-derived chromatin.

OBJECTIVE: The efficient uptake of dying cells by phagocytes is essential to the avoidance of chronic inflammation. Some human autoimmune responses are thought to be driven by autoantigens from apoptotic or necrotic cells. We analyzed the role of C1q and DNase I in the disposal of necrotic cell-derived chromatin because deficiencies in these serum factors predispose to the development of systemic autoimmune disorders, such as systemic lupus erythematosus. METHODS: Human necrotic peripheral blood lymphocytes were incubated in cell culture medium supplemented with various sera or serum components. Chromatin degradation was monitored by measuring the residual DNA content by flow cytometry. The uptake of necrotic cell-derived nuclei was analyzed by in vitro phagocytosis assays. RESULTS: Reconstitution of C1q-depleted serum with C1q strongly increased its ability to degrade necrotic cell-derived chromatin. Although C1q itself displayed no DNase activity, it strongly augmented the activity of serum DNase I. Whereas an excess of recombinant DNase I degraded chromatin in the absence of C1q, efficient uptake of the predigested material by monocyte-derived phagocytes required the presence of C1q. These data show that C1q and DNase I cooperate in the degradation of chromatin from necrotic cells. Furthermore, C1q was found to be necessary for effective uptake of degraded chromatin by monocyte-derived phagocytes. CONCLUSION: C1q or DNase I deficiencies may precipitate autoimmunity in humans by a mechanism similar to that of other molecules that are involved in the safe, efficient, and rapid disposal of dying cells.

Apoptosis↗
PubMed2003

Human peritoneal macrophages in culture: a model for studying inflammatory disorders in vitro.

In this study we characterized a model of human peritoneal macrophages maintained in culture for up to 48 h that can be used to study different functions of this cell population in vitro. The cells remained viable and functionally active over time, with well-preserved phagocytic properties. They expressed a macrophage marker, CD14. Once in culture, human peritoneal macrophages secreted C1q and nitric oxide in a pattern described in murine, guinea pig, and rat peritoneal macrophages. The described model can be used to study physiology and pathophysiology of peritoneal macrophages in vitro, offering all the advantages of the use of a human cell population.

Animals↗
PubMed1999

EMILIN, a component of the elastic fiber and a new member of the C1q/tumor necrosis factor superfamily of proteins.

EMILIN (elastin microfibril interface located protein) is an extracellular matrix glycoprotein abundantly expressed in elastin-rich tissues such as blood vessels, skin, heart, and lung. It occurs associated with elastic fibers at the interface between amorphous elastin and microfibrils. Avian EMILIN was extracted from 19-day-old embryonic chick aortas and associated blood vessels and purified by ion-exchange chromatography and gel filtration. Tryptic peptides were generated from EMILIN and sequenced, and degenerate inosine-containing oligonucleotide primers were designed from some peptides. A set of primers allowed the amplification of a 360-base pair reverse transcription polymerase chain reaction product from chick aorta mRNA. A probe based on a human homologue selected by comparison of the chick sequence with EST data base was used to select overlapping clones from both human aorta and kidney cDNA libraries. Here we present the cDNA sequence of the entire coding region of human EMILIN encompassing an open reading frame of 1016 amino acid residues. There was a high degree of homology (76% identity and 88% similarity) between the chick C terminus and the human sequence as well as between the N terminus of the mature chick protein where 10 of 12 residues, as determined by N-terminal sequencing, were identical or similar to the deduced N terminus of human EMILIN. The domain organization of human EMILIN includes a C1q-like globular domain at the C terminus, a collagenous stalk, and a longer segment in which at least four heptad repeats and a leucine zipper can be identified with a high potential for forming coiled-coil alpha helices. At the N terminus there is a cysteine-rich sequence stretch similar to a region of multimerin, a platelet and endothelial cell component, containing a partial epidermal growth factor-like motif. The native state of the recombinantly expressed EMILIN C1q-like domain to be used in cell adhesion was determined by CD spectra analysis, which indicated a high value of beta-sheet conformation. The EMILIN C1q-like domain promoted a high cell adhesion of the leiomyosarcoma cell line SK-UT-1, whereas the fibrosarcoma cell line HT1080 was negative.

Amino Acid Sequence↗
PubMed1994

Short-term kinetics of the humoral anti-C1q response in SLE using the ELISPOT method: fast decline in production in response to steroids.

Twenty four systemic lupus erythaematosus patients and 17 patients with other diagnoses were investigated regarding the presence of cells producing C1q reactive antibodies in peripheral blood mononuclear cells using the ELISPOT technique. These results were then compared with parallel serum levels of C1q reactive antibodies. Current production of anti-C1q was almost entirely confined to the systemic lupus erythaematosus group. Longitudinal analysis of anti-C1q ELISPOT positive patients showed rapid changes in the number of anti-C1q producing cells, but only slowly changing serum levels of the corresponding antibodies in response to glucocorticoids. In one systemic lupus erythaematosus patient prednisolone treatment had a selective effect on this autoantibody production, as the production of anti-C1q spot forming cells rapidly dropped to zero, at the same time as the number of total spot-forming cells showed only less change. In another patient, self-limiting connective tissue disease was associated with temporal occurrence of IgM anti-C1q. We believe, from these data, that the ELISPOT method for determination of current antibody production may be of particular value in longitudinal evaluation of disease course and therapeutic effects in systemic lupus erythaematosus and other rheumatic diseases.

Adult↗
PubMed1986

Fluorescent anti-immunoglobulin G assay of circulating immune complexes extracted with polyethylene glycol.

After a polyethylene glycol extraction which removes monomeric immunoglobulin G (IgG), circulating immune complexes were assayed by the FIAX fluorescence assay (Whittaker M. A. Bioproducts, Walkersville, Md.). The extraction portion of the procedure can be completed within a few hours after an overnight precipitation step, and the fluorescence assay takes about 0.5 h. The fluorescence assay is similar to the routine FIAX method for measuring IgG in cerebrospinal fluid except that a 10-microliter sample from sera is substituted for a 50-microliter sample. Good parallelism between endogenous immune complexes, monomeric IgG, and aggregated human globulin, along with good between-run precision (coefficients of variation, less than 10%), indicates that monomeric IgG calibrators from the kit could be used to standardize the assay. This standardization eliminates the need for aggregated human globulin, which is unstable and difficult to prepare. A reference range of 9 to 63 mg/liter followed a gaussian distribution. Correlation data indicate that the test provides information similar to the C1q-binding test (rho = 0.87; n = 30) but has better diagnostic sensitivity and better discrimination in the high range. Because of its simplicity, good reproducibility, and accessibility to equipment available in many laboratories, the method described here may be a preferred technique for measuring circulating immune complexes.

Antigen-Antibody Complex↗
PubMed2002

[Non-specific changes in the complement system in neoplastic processes].

The study using immunochemical and biological methods was concerned with assaying complement components C1q, C3, C4, and C5, C3 derivatives--C3a and, C3(H2O), C1ing control protein, hemolytic activity (CH50), total proteolytic activity and regulatory immune complexes in sera from patients with cancer of the stomach, breast and ovary, subjects at risk of cancer and healthy donors. Neoplasia was associated with lowered levels of intact C3 and C1ing matched by high concentrations of C3a, C1q and C4. Hemolytic activity (CH50) was increased against the background of relatively higher total proteolytic activity both in healthy subjects and cancer patients. Significant decrease in C1ing concentration may be used as an additional biochemical prognosticator in breast cancer.

Biomarkers, Tumor↗