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PubMed1993

Evaluation of in vivo immune complex formation and complement activation in patients receiving intravenous streptokinase.

The usefulness of several different methods for detecting immune complex formation and complement activation in the circulation were applied to samples from patients receiving intravenous Streptokinase therapy for myocardial infarction. Streptokinase is a foreign antigen and can cause immune reactions. We collected samples from 13 patients, before Streptokinase administration (baseline), at the end of infusion (1 h), 12 h later and on day 7. We measured IgG containing immune complexes (IgG-IC), free C3d and antibodies to Streptokinase by ELISA, and CR1, C3d and C4d on erythrocytes by flow cytometric assay. Antibodies to Streptokinase are common, as all but two of the patients had measurable antibody levels. During Streptokinase treatment there was a drop in antibody levels, most prominent in those patients who had high baseline levels. At the same time increased levels of free C3d and erythrocyte-bound C3d were observed. After 12 h free C3d was usually back to baseline level, but C3d on erythrocytes was still raised. These data indicate the formation of Streptokinase immune complexes in patients with high Streptokinase antibody levels, and show that these complexes are cleared rapidly from the circulation, leaving more persistent signs of complement activation. We conclude that free C3d is a good indicator of ongoing complement activation, whereas C3d on erythrocytes indicates that complement activation has recently taken place.

Antibodies↗
PubMed1994

Reactive oxygen product formation by human neutrophils as an early marker for biocompatibility of dialysis membranes.

Production of reactive oxygen intermediates (ROI) by neutrophils (PMN) in vivo was examined by a whole blood assay using dichlorofluorescein-diacetate (DCFH-DA) in 10 patients each dialysed consecutively with two different dialyser membranes. Haemodialysis (HD) with cuprophan membrane (CM) led to a significantly (P < 0.001) more pronounced ROI production by PMN (2.4 +/- 0.5-fold increase in intracellular oxidation of DCFH-DA) compared with HD with polysulfone membranes (PM; 1.5 +/- 0.2-fold). HD with CM induced a decrease in PMN count by about 90%, whereas PM induced a decrease by only 25% (P < 0.001). In CM patients maximal ROI production coincided with the nadir in PMN count. All patients dialysed with CM showed a clear increase in serum levels of Bb fragments, whereas PM-dialysed patients did not. In this respect, however, no clear time relationship was seen to the kinetics of ROI production, nor to the disappearance of neutrophils from the circulation. Evaluating a direct effect of the dialysis membranes on PMN demonstrated that incubation of neutrophils with hollow fibres of the CM but not of the PM in the absence of plasma induces significant ROI production by PMN. Our study thus indicates that ROI production by PMN during HD correlates to membrane biocompatibility. Furthermore, one might speculate that also independently from but perhaps in addition to complement activation, reactive oxygen products are critically involved in the generation of haemodialysis-associated neutrophil emigration.

Adult↗
PubMed2006

Presence of plasma complement regulatory proteins clusterin (Apo J) and vitronectin (S40) on circulating immune complexes (CIC).

The complement regulatory (CR) proteins clusterin and vitronectin bind to the membrane attack complex (MAC) and thus prevent cytolysis. In this report, we demonstrate the presence of both of these CR proteins on MAC bound to circulating immune complexes (CIC). We measured the amount of clusterin and vitronectin on MAC in plasma, also referred to as soluble MAC (SMAC), as well as on MAC bound to CIC (MAC-CIC), using antibody directed to polymerized C9 in systemic lupus erythematosus (SLE) patients. We observed a strong correlation among the quantities of SMAC and MAC-CIC. The amount of both clusterin and vitronectin associated with MAC-CIC was two- to threefold higher in comparison to the SMAC. Patients with high levels of clusterin and vitronectin demonstrated renal involvement. We hypothesize that these complement regulatory proteins besides regulating the insertion of MAC play other critical roles, in disease pathogenesis.

Antigen-Antibody Complex↗
PubMed1992

Changes in immunologic response in tonsillectomized children. I. Immunosuppression in recurrent tonsillitis.

The possible immunoregulatory role of the tonsils was studied by determining immunoglobulins IgG, A, M, E and factors C'3, C'4 and PFB of the complement system before and after tonsillectomy. The synthesis in vitro of IgG and IgM by lymphocytes stimulated with pokeweed mitogen was also measured. There were statistically significant differences between pre and post-operative levels of serum IgG, IgA and IgM, which decreased after surgery. Practically no change in the mean values of IgE and no significant differences in the levels of serum C'3, C'4, and PFB, were found. The in-vitro synthesis of both immunoglobulins (IgG, IgM) by lymphocytes increased significantly after tonsillectomy. Our results suggest that not only does tonsillectomy have no counterproductive effect on the immune system, but that, on the contrary, it seems to improve the immune response, since it appears to unblock the suppression to which the immune system was subject.

Child↗
PubMed1991

n-3 fatty acids and acute-phase proteins.

The aim of this study was to determine the effects of n-3 fatty acids on acute-phase proteins and response. Healthy male volunteers were submitted to standard bicycle ergometry once without supplementation and a second time after 3-weeks supplementation with highly purified n-3 fatty acids (1.75 g eicosapentaenoic acid and 1.05 g docosahexaenoic acid per day). Acute-phase proteins (immunoglobulin M, complement C4, haptoglobin, C-reactive protein, alpha 2-macroglobulin, coerulopasmin, fibrinogen, alpha 1-glycoprotein) were measured before, immediately after, 24 and 72 h after exercise. There were significantly lower values of immunoglobulin M (pre-exercise and at 72 h) and alpha 2-macroglobulin (pre-exercise) when cross-sectionally comparing the baseline data with and without n-3 supplementation. Longitudinal comparisons show that the ergometric test induced a discrete acute-phase reaction, which is evident with and without n-3 fatty acids. Yet the kinetics of the response seem to be altered by n-3 supplementation. The relative increase of most acute-phase proteins is numerically larger and the rise persists longer, which is particularly evident for fibrinogen and alpha 1-glycoprotein. The findings suggest that n-3 fatty acids lower acute-phase proteins at baseline and alter the pattern of change following acute exercise.

Acute-Phase Proteins↗
PubMed1981

MHC specified lymphocyte activating and suppressor activating determinants in human mixed lymphocyte reactions.

We have shown (1) the presence of HLA-linked Sad/s on a homozygous typing cell (HTC), FPA (8W321). When we used it to type the P family, which included an HLA-B/DR recombinant sibling, its genes mapped towards the HLA-B-A end of the HLA haplotype separate from HLA-D/DR and was found to be associated with HLA-Bw35 homozygosity; (2) this same recombinant maps the C4 complement genes on the HLA-D/DR end of the chromosome away from HLA-B; (3) that the suppressor T cell subpopulation which was activated by the Sad of this consanguineous HTC FPA was left behind after separating the OKT4 positive cells with a monomorphic monoclonal anti-T-cell antibody (OKT4). These OKT4 positive cells reacted normally in MLC to the FPA Lad Fes 6; (4) that at least part of the genetic control of suppressor recognition is outside the HLA complex.

Chromosome Mapping↗
PubMed1984

Factor I deficiency and C3 nephritic factor: immunochemical findings and association with Neisseria meningitidis infection in two patients.

The complement system was examined in two patients with systemic Neisseria meningitidis infections, both of whom had reduced or nondetectable CH50 as analysed by both pathways. C3 measured by conventional technique revealed 19% anti-C3c-reactive protein in the plasma of patient 1 and 3% in patient 2. Patient 1 had circulating C3b but no detectable C3c, C3d, or C4d, whereas patient 2 had normal levels of C3c and C4d and strongly elevated levels of C3d. Factor B analysis revealed no demonstrable native factor B and small amounts of Bb in patient 1 and normal concentration of native factor B plus trace amounts of Bb in patient 2. The depletion of C3 in both patients was due to uncontrolled activation caused by complete factor I deficiency (patient 1) and circulating C3 nephritic factor (patient 2). Both parents of patient 1 had factor I concentrations below (mean-2 SD) that seen in normal healthy individuals (n = 20). Circulating immune complexes (IC) were demonstrated in patient 1 only, whereas serum from both patients had strongly reduced capacity to solubilize preformed IC.

Adolescent↗
PubMed1991

Age of onset in vitiligo: relationship with HLA supratypes.

HLA class I (A, B, C), class II (DR, DQ) histoglobulins and HLA class III (C4A, C4B and Bf) complement factors were analysed in 87 patients with vitiligo and in controls. Two HLA supratypes seem to mark different age of onset of vitiligo: HLA-BfS, C4A3, C4B1, DR5 (W11), DQW3 is characteristic of the pediatric form; while HLA-BfS, C4A3, C4B1, DR7, DQW2 marks the adult form of disease. The importance of defining HLA supratype, not single alleles, is discussed.

Adolescent↗
PubMed2004

Histological analysis of late renal allografts of antidonor antibody positive patients with C4d deposits in peritubular capillaries.

The association of humoral immunity with late renal allograft dysfunction has recently been recognized, and many reports have revealed C4d deposits in peritubular capillaries (C4d in PTC), and the presence of serum antidonor HLA antibody in patients suffering from graft dysfunction, long time after transplantation. In this study, morphological changes in renal allograft biopsies more than 1 year after transplantation in 14 patients with C4d in PTC and serum antidonor antibody were investigated for the presence of chronic rejection (CR). In addition to the light microscope study, an electron microscope study was done to evaluate the multilayering of the peritubular capillary basement membrane (MLPTC). Histologically, only seven of 14 patients met the criteria of CR, and 71.4% (5/7) of CR patients had episodes of acute humoral rejection (AHR), coexisting with acute tubulointerstitial rejection. Peritubular capillaritis was observed in all patients, although it differed in severity. Transplant glomerulitis and interstitial inflammation were also observed in many patients: 71.4% (10/14) and 92.9% (13/14) respectively. MLPTC was observed in 12 patients (85.7%), but the severity of the MLPTC did not reflect the severity of peritubular capillaritis or any other histological features. The long-term outcomes of the patients CR, especially those with episodes of AHR, were poor, and two of them lost their graft functions. On the other hand, patients without CR had relatively favourable outcomes. In conclusion, we confirmed the diverse morphological changes of late renal allografts, which cannot be categorized as chronic humoral rejection (CHR), and such patients who do not have typical morphological changes such as CHR, should be followed-up on a long-term basis in order to clarify the significance of C4d on PTC in late renal allografts.

Adolescent↗
PubMed2004

C4d and/or immunoglobulins deposition in peritubular capillaries in perioperative graft biopsies in ABO-incompatible renal transplantation.

We evaluated 0 h and/or 1 h graft biopsy specimens from 14 recipients in ABO-incompatible renal transplantation using immunofluorescence for C4d, IgG, and IgM. All 0 h biopsy specimens revealed negative C4d, IgG, and IgM deposition in peritubular capillaries (PTC). In contrast, 8 of 14 1 h biopsy specimens revealed a positive C4d deposition in PTC. Eight specimens revealed positive IgM staining and seven of them had both C4d and IgM depositions. Three specimens had C4d, IgM, and IgG depositions in PTC. Three of eight patients with C4d deposition and two of six patients without C4d deposition in the 1 h biopsy group suffered from acute rejection within 1 month of transplantation. These findings suggest that complement fragments and immunoglobulin deposition in PTC in ABO-incompatible renal grafts can start soon after reperfusion, although acute rejection may or may not develop.

ABO Blood-Group System↗
PubMed2004

Pathological study on the relationship between C4d, CD59 and C5b-9 in acute renal allograft rejection.

In order to evaluate the activation or inhibition of the later phases of classical complement cascade in renal allograft presenting with acute rejection, particularly with C4d deposition on the peritubular capillary (PTC), we observed the expression of CD59 and C5b-9 on the PTC. Subjective cases were divided into two groups, an acute rejection group, of 4 males and 6 females, and a normal donor group, of 5 males and 5 females. Renal biopsies were performed at the onset of acute rejection and at the transplant operation, before reperfusion. C4d deposition on PTC was found in three of 10 cases (30%) with biopsy proven acute rejection, whereas CD59 on PTC was positively expressed in all of the rejection cases. Although C5b-9 was not observed on PTC in the acute rejection group, it was intensively deposited on the tubular basement membrane (TBM) in five cases, including the three with positive C4d on PTC. In the normal donor group, CD59 on PTC was intensively observed, whereas C5b-9 was weakly expressed on TBM. CD59, a complement regulatory factor, works as an inhibitory factor against the formation of C5b-9, a membrane attack complex. From our data, we noted the dissociation between the depositions of C4d and C5b-9 on PTC. The substantially expressed CD59 on PTC may affect this dissociation between C4d and C5b-9 on PTC. The intensive deposition of C5b-9 on TBM in acute rejection cases may suggest an independent immunological injury attacking tubular cells.

Acute Disease↗