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PubMed1990

Blood-borne collagenous debris complexes with plasma fibronectin after thermal injury.

Plasma fibronectin augments the clearance of blood-borne foreign and effete complexes by mononuclear phagocytes. The release of a "gelatin-like" ligand into plasma after thermal injury has been reported. We quantified the release of this collagenous debris from thermally injured skin, and its potential interaction with soluble fibronectin in plasma using anesthetized rats. Collagen-like material debris in the plasma was detected by assay of hydroxyproline. Fibronectin was measured by a double antibody enzyme-linked immunosorbent assay (ELISA) technique. Over a 24-hour postburn interval, plasma hydroxyproline increased from 6.7 +/- 0.6 micrograms/mL to a maximum of 19.0 +/- 3.3 micrograms/mL at 60 minutes postburn, and normalized by 6 hours. A direct correlation existed between the magnitude of burn injury and the increase in plasma hydroxyproline. In parallel, plasma fibronectin declined over a 15-minute to 2-hour period postburn, and normalized by 3 to 4 hours with rebound hyperfibronectinemia observed at 24 hours. The elevation in total plasma hydroxyproline was not due to an increase in plasma Clq (zero time, 26.2 +/- 1.4 micrograms/mL; 60 minutes, 23.9 +/- 1.1 micrograms/mL). Tracer studies with 125I-fibronectin showed that the acute decline of plasma fibronectin was due to its uptake by the liver and binding to sites of tissue injury. Total hydroxyproline in extracts of burn skin, used as an index of soluble collagenous material, rose from 15 +/- 3.3 micrograms/g skin at zero time to 129.3 +/- 43.7 micrograms/g skin by 5 minutes postburn, with a decline to 38 +/- 22 micrograms/g skin by 24 hours. The formation of circulating fibronectin-gelatin complexes in vivo was documented by cross-immunoelectrophoresis coupled with autoradiography using 125I-gelatin as a model ligand. Thus, collagenous tissue debris from burned skin may enter the plasma after thermal injury and directly complexes with soluble fibronectin before hepatic phagocytic clearance.

Animals↗
PubMed1989

Zidovudine-induced fever.

Zidovudine (3'-azido-3'deoxythymidine, AZT, Retrovir) is the first antiretroviral drug to demonstrate clinical efficacy for symptomatic human immunodeficiency virus infection. In a large, placebo-controlled trial, nausea and hematologic toxicity, but not fever, occurred more frequently in zidovudine- than in placebo-treated patients. However, in an open label study, fever severe enough to halt zidovudine administration occurred in 10% of 70 acquired immune deficiency syndrome (AIDS) patients receiving the drug. We now describe three AIDS patients with severe zidovudine-induced fever in whom other causes of fever were excluded. Zidovudine-induced fever was confirmed in each case by drug rechallenge. Using an enzyme immunoassay, we detected IgM antibodies directed against a zidovudine-serum protein conformational determinant in one of these three patients. Neither IgG nor IgM anti-zidovudine antibodies were present in sera from the other two patients with zidovudine fever, from four AIDS patients who discontinued zidovudine for reasons other than fever, or from five AIDS patients who never received zidovudine. Zidovudine may cause fever as a severe adverse effect in patients with AIDS. Either type III or type IV hypersensitivity may mediate this reaction.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

[Velocity of nerve conduction in children and adolescents with type I diabetes mellitus: clinical, metabolic and immunologic correlations].

Clinical, metabolic, neurophysiologic and immunological data were obtained in a group of 50 patients with type I diabetes mellitus Results were compared with those obtained in 30 healthy subjects of comparable age. M.N.C. (median nerve conduction) velocities and sensitive latency were observed to be significant lower in the diabetic patients rather than in the controls. These abnormalities were correlated with the duration of diabetes rather than with the glucose control. The positivity for circulating immune complexes was found to be associated with a significant reduction of median sensory nerve conduction velocity. There results suggest that in addition to metabolic, genetic, vascular and hormonal abnormalities also immunologic factors may play a role in the pathogenesis of diabetic neuropathy.

Adolescent↗
PubMed1985

[Cytotoxicity induced by the serum of patients with AIDS and at high risk of AIDS against cells infected with Epstein-Barr virus].

Serologic reactivity against EBV-infected lines was assayed in patients with AIDS (n = 4) or the AIDS related complex (AIDS-RC) (n = 46) residing in Argentina. Anti-VCA serology was comparable to that of controls. However sera from AIDS and AIDS-RC could induce antibody dependent cell mediated cytotoxicity (ADCC) to EBV-infected cell lines (P3HRIK and Raji). ADCC activity could be recovered in the high molecular weight fractions of AIDS and AIDS-RC sera. ADCC was observed in sera with high levels of PEG precipitable material (PEG-pp) but was unrelated to the presence of complement-fixing immune complexes (Clq-F) or to anti-VCA titers. Fc receptor (FcR) bridging between target cells FcR and effector cells FcR may play a role in the outcome of total ADCC.

AIDS-Related Complex↗
PubMed1988

The binding of native DNA to the collagen-like segment of Clq.

Our study was undertaken to determine if native DNA (dsDNA), which is known to bind to collagen, also binds to the collagen-like segment of Clq (CLS). Three methods were employed to demonstrate the binding of dsDNA to CLS: (1) Six human sera and a mouse monoclonal antibody to dsDNA were employed in an enzyme linked immunosorbent assay to detect CLS bound dsDNA. When applied to CLS bound dsDNA, sera with antibodies to dsDNA and monoclonal antibody to DNA yielded mean OD values of greater than or equal to 0.6, significantly higher than those values obtained from control experiments (mean OD less than or equal to 0.2, p less than or equal to 0.003). (2) In a solid phase immunoassay radiolabelled DNA (3H DNA) was exposed to increasing amounts of solid phase adherent CLS. The binding of 3H DNA to the solid phase was substantially greater (more than a 30-fold increase) when the solid phase had been precoated with CLS. (3) dsDNA binding to CLS was demonstrated further by incubating electrophoretically resolved CLS with dsDNA and localizing the bound dsDNA by ethidium bromide staining. Our results indicate the dsDNA binds to CLS. Since CLS is the binding site for Clr and then Clr2Cls2, molecules which bind to CLS, such as dsDNA, could be important factors affecting Cl activation.

Collagen↗
PubMed1986

Antilymphocytic antibodies and marrow transplantation. VIII. Recipient conditioning with Clq-affine monoclonal anti-pan T antibodies prevents GVHD in homozygous fully mismatched mice.

An approach to suppressing secondary disease with antibodies was studied that differed from conventional antibody treatment of donor marrow in vitro. It consisted of the selection of anti-Thy-1 antibodies with high affinity for Clq, the first subunit of the complement cascade, and a single injection of such antibodies into prospective irradiated marrow recipients. Monoclonal mouse IgM and rat IgG 2c antibodies of high titers in complement-dependent test systems but with low affinity for Clq caused little immunosuppression. Monoclonal rat IgG2b or mouse IgG2a anti-Thy-1 antibodies with high affinity for Clq prevented acute and chronic mortality of graft-v-host disease (GVHD), however, when injected in irradiated CBA or AKR mice prior to C57BL/6 spleen and/or bone marrow cell transfusion. This treatment simultaneously suppressed residual host-v-graft reactivity of the irradiated mice, so that permanent hematopoietic engraftment ensued even at 5 or 6 Gy. Full chimerism and specific tolerance were obtained. Primary immune response to SRBC was clearly depressed in the chimeras; secondary immune response was not. Clearance of T cell antibody activity (greater than 6 days), timing, and dose of injected antibody, as well as other modalities of the conditioning treatment that may have contributed to the remarkable immunosuppression, are discussed.

Animals↗
PubMed1988

[Clinical, immunologic and therapeutic aspects of endangiitis obliterans].

In the period of 1975-1983 twenty-three patients with thromboangiitis obliterans were examined at the Surgical Clinic of the Medical Academy of Magdeburg. The diagnosis was established clinically, angiographically histologically and immunologically. In 7 out of 12 patients histology revealed inflammatory vascular alterations including lymphocyte infiltrates throughout the entire vessel wall and also in the perivascular area. Immunohistology showed in 10 out of 15 patients segmental granular fluorescence identifiable as deposits of IgM and IgG. In 6 cases a complement formation was found. The endangiitis group revealed more frequent and increased immune complexes concentrations. Circulating immune complexes were established by phase-locked radio-immunoassay. The therapy is depended on the localization of the obliteration and can be a lumbar sympathectomy or a vascular reconstruction.

Adult↗
PubMed1977

Glomerular lesions in patients with asymptomatic persistent andorthostatic proteinuria discovered on routine medical examination.

The incidence of asymptomatic proteinuria in young healthy men entering the army service in Singapore was 0.94%; 0.56% had intermittent orthostatic proteinuria and 0.38% with persistent proteinuria. Renal biopsies from 45 cases with persistent proteinuria and 10 cases with orthostatic proteinuria were studied by light microscopy, electron microscopic and immunofluorescent antibody techniques. Three cases with orthostatic proteinuria showed a minimal lesion ('Nil'), and 7 a minimal lesion with increased centrilobular mesangial matrix and mild focal and segmental mesangial hypercellularity. Focal and segmental capillary loop changes were seen in two cases. No immunoglobulin deposits were found in orthostatic proteinuria. A raised anti-streptolysin O titer was found in 3 cases. 13.3% of cases with persistent proteinuria showed a minimal lesion ('Nil'); 66.6% a minimal lesion with increased centrilobular mesangial matrix and mild focal and segmental mesangial hypercellularity: Focal global sclerosis, focal segmental sclerosing glomerulonephritis and diffuse proliferative GN (mesangial hypercellularity) were each found in 6.7% of patients in this group. Focal and segmental changes in capillary loops were found in 30% of cases. Changes in visceral epithelium such as the appearance of cytoplasmic swelling, vesicles and dense aggregates, and areas of focal foot process fusion were common findings. Mesangial deposits of IgA were found in 34.3%, with an IgA-IgG-beta1C globulin combination in 28.6% of cases. IgM-beta1C globulin was present in 5.7% of cases with persistent proteinuria. Early complement components, C1q and C4, and IgA secretory piece were absent. A raised antistreptolysin O titer was found in 25% of cases. The changes inthe glomeruli may represent the end or healing stages of an early bout of glomerulonephritis. Changed hemodynamic responses on assuming an upright position may play a role in the loss of protein across the glomerular basement membrane in patients with orthostatic proteinuria.

Adolescent↗
PubMed1986

Autoantibody profiles in juvenile arthritis.

Serologic and correlational testing was performed in a series of 65 patients diagnosed as having juvenile arthritis (JA) and in 21 age matched controls to detect the presence of antinuclear antibodies (ANA), antibodies to ssDNA, IgM and IgG rheumatoid factor (RF), immune complexes (IC) and antibodies to bovine type I and human type II collagen. ANA were found in 51% of the JA patients; the highest incidence (75%) was noted in the pauciarticular onset disease group. Low levels of anti-ssDNA antibodies were detected in 22% of the patients, all of whom had active disease. IgM RF was detected in 35% of the JA patients but only 6% of patients had IgG RF. Similarly, about one fourth of the JA patients had IC detected by the Clq assay. Antibodies to bovine type I and human type II collagen were noted in about 12% of the JA patients.

Adolescent↗
PubMed1986

The binding of dsDNA and ssDNA to human types I, II and IV collagens.

Our study was undertaken to determine if dsDNA and ssDNA, which are known to bind to bovine collagen and to glomerular basement membrane, also bind to purified human types I, II and IV collagens. Four human sera with antibodies to dsDNA and 4 human sera with antibodies to ssDNA, when employed in an enzyme linked immunosorbent assay, detected DNA binding to the solid phase only when the solid phase had been precoated with collagen. Mean optical densities (OD) of .978, 1.062 and 1.033 for dsDNA binding to types I, II and IV collagens, respectively, were substantially higher than the mean OD value of .177 obtained when dsDNA was applied to the noncollagen coated solid phase. Similarly, mean OD values of .664, .526 and .902 for ssDNA binding to types I, II and IV collagens, respectively, were higher than the mean OD value of .147 obtained when ssDNA was applied to the noncollagen coated solid phase. The affinity of DNA for collagen could be an important factor contributing to the localization of DNA-anti-DNA complexes in target tissues.

Animals↗
PubMed1986

Detection of C-reactive protein, streptolysin O, and anti-streptolysin O antibodies in immune complexes isolated from the sera of patients with acute rheumatic fever.

Circulating immune complexes (IC) of 42 patients with acute rheumatic fever from Santiago, Chile, were studied. The complexes were isolated by polyethylene glycol precipitation and were analyzed for antibodies, antigens, and C-reactive protein. We found the complexes to be enriched in antibody to streptolysin O, particularly in the group of patients with elevated levels of IC. IgM was the predominant class of Ig present in the complexes. Western blots from 12 patients to detect antigens in the complexes showed proteins of m.w. 50,000, 60,000, and 69,000, consistent with the polypeptides of streptolysin O. Such antigens were absent in the complexes from patients with post-streptococcal glomerulonephritis and pharyngitis. Eluted antibodies from these protein bands on the nitrocellulose sheets reacted with the streptolysin O in Western blots and neutralized the hemolytic activity of streptolysin O in a microhemolysin assay. In addition, isolated complexes from several sera showed the presence of C-reactive protein bound to complexes. In vitro experiments demonstrated that [125I]C-reactive protein was not precipitated by polyethylene glycol either alone or when added to monomeric IgG, whereas it precipitated significantly when added to aggregated IgG. The detectable C-reactive protein in isolated complexes and sera samples increased after treatment with sodium dodecyl sulfate. These data suggest that circulating immune complexes in acute rheumatic fever contain streptolysin O and its antibody and raise interesting questions regarding the pathogenetic significance of C-reactive protein in the complexes.

Antigen-Antibody Complex↗
PubMed1986

Administration of monoclonal anti-Sm antibody prolongs the survival and renal function of MRL-lpr/lpr mice.

The repeated administration of a monoclonal anti-Sm antibody (KSml) resulted in a significant prolongation of life in MRL-lpr/lpr lupus mice with a 50% mortality of 36 weeks compared with 18-24 weeks in the control groups. Control animals injected with APC11 (a myeloma protein of the same isotype) lived no longer than an untreated group. In addition the renal function as assessed by blood urea levels was less impaired in the KSml-injected mice than in the controls. All KSml-injected mice showed the presence of circulating anti-Sm antibodies which had a different Sm polypeptide binding specificity from that of the injected monoclonal antibody; the increased prevalence of these antibodies compared to the control mice (10-30%) suggested that the anti-Sm antibody response had been induced. The increased longevity in the KSml-treated animals was not associated with alterations in the anti-dsDNA antibody response. The data suggest that administration of anti-Sm antibodies modifies the course of murine lupus.

Animals↗
PubMedDate not supplied

[The role of the immunoglobin G "hinge" region in heat aggregation and activation of complex-formation].

A high degree of correlation between the capability of subclasses of human immunoglobulins G to form aggregates due to thermal treatment, and their complement-binding activity was established. On the basis of the experimental data obtained by the methods of light scattering, circular dichroism, microcalorimetry, it was supposed that "hinge" region of immunoglobulins G participates in the initial stage of thermal aggregation and in the activation of the process of complement binding.

Binding Sites, Antibody↗
PubMed1987

Cryoglobulinemia induced by monoclonal immunoglobulin G rheumatoid factors derived from autoimmune MRL/MpJ-lpr/lpr mice.

A MRL strain bearing the autosomal recessive mutant gene, lpr (lymphoproliferation), spontaneously develops, in addition to a lupus-like syndrome, unique serological and pathological manifestations. Production of high titers of IgG rheumatoid factors (RF) may be related to the formation of extremely large amounts of cryoglobulins and the development of tissue lesions such as necrotizing polyarteritis, arthritis, and glomerulonephritis. To analyze more directly the relationship of IgG RF to the development of cryoglobulins and tissue injuries, we have established four monoclonal IgG RF secreting hybridomas from unimmunized MRL-lpr/lpr mice and determined their pathogenic effects in normal strains of mice. All the monoclonal IgG RF obtained in this study were of the IgG3 subclass and generated cryoglobulins. However, the fact that not only IgG3 Rf monoclonals but also four of five non-RF IgG3 monoclonals were able to form cryoglobulins, which were composed exclusively of each IgG3 monoclonal, indicates that the IgG3 molecule has a unique physicochemical property to self-associate via nonimmunological interaction and the ability to form cryoglobulins. When the in vivo pathogenic activities of these IgG3 RF and non-RF monoclonals were examined, three of IgG3 RF monoclonals with the specificity to IgG2a were able to induce extensive pathologic manifestations including peripheral vasculitis and glomerulonephritis characteristic of patients with cryoglobulinemia. Our results indicate that the IgG3 itself, independently of its specificity, could be a potential source of cryoglobulins and IgG3 RF, combined with its activity of cryoglobulin formation, may play a significant role in the development of glomerulonephritis and cutaneous vascular lesions of ears and foot pads observed frequently in aged MRL-lpr/lpr mice.

Animals↗