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PubMed1989

[Pemphigus herpetiformis--the value of simple diagnostic measures].

Herpetiform pemphigus is a rare variety of pemphigus vulgaris. Although the final diagnosis requires thorough clinical, histological and immunological investigations, there are simple examinations which may be carried out at once (such as assessment of blister stability, negative Nikolski's sign, predominance of eosinophils, spongiotic and non-acantholytic epidermal cells in the Tzanck smear). These ad hoc findings may help the practising dermatologist to tell herpetiform pemphigus from other blistering diseases. We discuss and evaluate the various diagnostic procedures regarding herpetiform pemphigus.

Aged↗
PubMed1989

[Atopic dermatitis. I. Characteristics of the clinical course and state of the immune status in relation to the initial level of serum IgE].

Altogether 97 patients with atopic dermatitis have been examined to follow this relationship, 72 patients presented with disseminated efflorescence, 25 patients with local rash. Measurements of immunoglobulins A, M, G, and D, of the C3c complement components, of the total and allergen-specific IgE C4, inactivators have been carried out, as well as of the total lymphocyte, B lymphocyte, and CD3+, CD4+, and CD8+ lymphocyte subpopulations; the lymphocyte response to ConA mitogenic stimulation has been also under study. The patients with normal and elevated levels of IgE differed by the clinical picture of the disease and by case histories, as well as by the immunity parameters and by the results of zaditen therapy. Cases with very low IgE levels may be indicative of alternative pathogenetic mechanisms.

Adolescent↗
PubMed1985

Suboptimal C3b/C3bi deposition and defective yeast opsonization. I. Evidence for the absence of essential co-factor activity.

Defective yeast opsonization in sera with no demonstrable abnormality of known complement components is associated with the absence of inactivity of a co-factor which enhances the deposition of C3 fragments (C3b/C3bi) derived from both classical and alternative pathways of complement activation. The factor binds strongly to zymosan at 4 degrees C and loses its biological activity completely when heated for 30 min at 56 degrees C but not when similarly heated at 50 degrees C. Sera with defective deposition of C3 fragments may be readily corrected with small quantities of sera having normal function. Sera with the defect do not correct other similar sera.

Adult↗
PubMed1988

Glomerular inflammation: a consequence of sequential challenge of the rat mesangium with particulate macromolecules.

Imposil pretreatment (50 mg/100 g bodyweight) of male Sprague-Dawley rate (100-150 g), 24-48 h before an albumin-coated latex challenge resulted 24 h later in markedly reduced mesangial endocytosis of latex, compared with control animals receiving latex-albumin alone. This reduced capacity to ingest latex was associated with increased glomerular infiltration by Ia+ macrophages and mesangial localisation if immunoglobulins and complement C3c. In sharp contrast, pretreatment with albumin-coated latex had little effect on the subsequent mesangial uptake of Imposil. In this reverse situation macrophage infiltration was minimal, immunoglobulin deposition was similar to that in untreated control animals, and C3c was not detectable. Similarly, extending the interval between Imposil pretreatment and albumin-coated latex challenge up to 144h resulted in only minor infiltration by Ia+ macrophages and immunoglobulin localisation without accompanying C3c deposition, even though mesangial latex uptake was still limited. These observations demonstrate the consequences of secondary challenge following mesangial impairment due to a predisposing insult. Glomerular inflammation was dependent upon the timing and nature of the sequential challenge. The results support the concept that mesangial impairment following an initial insult may be a major factor in the predisposition to some forms of human glomerular inflammation.

Animals↗
PubMed1985

Neutrophils express a receptor for iC3b, C3dg, and C3d that is distinct from CR1, CR2, and CR3.

In the present study we examined human neutrophils for the expression of a receptor capable of binding C3dg and defined the relationship of this receptor to those that have been previously described, namely CR1, CR2, and CR3. C3dg was isolated from serum depleted of plasminogen, supplemented with 20 mM Mg++, and incubated at 37 degrees C for 6 to 8 days. The purified protein was homogeneous when analyzed by polyacrylamide gel electrophoresis and exhibited an apparent m.w. of 41,000. C3dg was polymerized by treatment with dimethyl suberimidate, and the dimer was isolated by gel filtration. Binding of both monomeric and dimeric 125I-labeled C3dg to neutrophils was saturable, and the latter ligand bound to an average of 12,400 sites/cell among nine normal individuals. At 4 degrees C, bound monomeric C3dg dissociated from neutrophils with an average t1/2 of 30 min, whereas dimeric C3dg dissociated with a t1/2 in excess of 120 min. Specific binding of multimeric C3dg was cation independent and was competitively inhibited by molar concentrations of iC3b and C3d that were equivalent to the inhibitory concentrations of unlabeled C3dg; C3b was less able to compete with C3dg for binding to these sites. The capacity of this neutrophil receptor to bind iC3b, C3dg, and C3d suggested its possible identity as CR2 or CR3. However, no specific binding to neutrophils of 125I-labeled HB-5 monoclonal anti-CR2 was detected. Furthermore, uptake of 125I-labeled C3dg was not inhibited by saturating concentrations of rabbit anti-CR1, anti-Mac-1, or OKM10. Thus, a receptor resides on neutrophils that binds the C3d region of iC3b and C3dg and is distinct from CR1, CR2, and CR3.

Animals↗
PubMed1988

Scanning electron microscopy, X-ray microanalysis and immunohistochemistry on worn soft contact lenses.

The deposits accumulated on the surfaces of soft contact lenses are a cause of problems for the wearer of these lenses, as the deposits are never completely removed by the available washing solutions. Therefore it appears of interest to investigate the composition of these deposits. In this paper we review the major findings in the literature and, in addition, present our personal experience. We have studied new, continuously and daily worn soft contact lenses by scanning electron microscopy (SEM), X-ray microanalysis and immunohistochemistry. We have carefully evaluated preparative methods, and we can conclude that SEM and X-ray microanalysis are best carried out on unfixed, air-dried lenses. The deposits present consist mainly of mucus, especially on the tarsal side of the lenses. Chloride and potassium, coming from the tear fluid, as well as sulfur, derived from proteins, were found. Calcium was very rarely detected. IgG, IgA, IgE and C3c complement fractions were found only on the outer surfaces and not within the lens. We believe that the best characterization of the deposits is achieved by means of correlative techniques on the same lens. In fact, this approach integrates morphology and composition.

Contact Lenses, Hydrophilic↗
PubMed1987

Specific immunotherapy in hay fever.

The observation included 120 patients suffering from hay fever (HF) in age 18-58. In 77 of them specific immunotherapy (SI) with pollen vaccine was applicated through 3 consecutive years, while 43 patients remained without this form of therapy, as a control group. SI was efficient in 47% of treated patients, and in these cases IgE value came back to normal value, the IgG level increased and suppression of skin test to pollen allergens was observed. In 17% of treated patients side effects appeared during SI and together with exacerbation of HF, an increase of skin reaction to pollen allergens was noted.

Adolescent↗
PubMed1987

[Quantitative determination of proteins in the contents of pseudocysts of the maxillary sinus].

The factors C 3c and C 4 of the complement system, the protease inhibitor alpha-1-antitrypsin (AAT) as well as the immunoglobulins IgA, IgG, IgM in the fluid of cysts of maxillary sinus were determined by means of single radial immunodiffusion. The concentration of these proteins was compared with the concentration in the serum obtained simultaneously. A decrease of C 3c, C 4 and AAT and an increase of IgA and IgG in fluid are indicators of active participation of the mucosa in defence processes.

Complement C3↗
PubMed1983

Heterogeneity in electrophoretic mobility of C3-derived molecules expressing D but not C-epitopes following in vivo activation of the complement system.

Four different populations of C3-derived molecules expressing D but not C epitopes were identified following in vivo activation of the complement system. The four molecular forms, differing in electrophoretic migration velocity, were assigned the nos. 1, 2, 3 and 4 after decreasing electrophoretic mobility. Analysis of the time-dependent changes in the relative concentration of the different molecular forms demonstrated an increase in the plasma concentration of population 4 and a decrease of populations 2 and 3, whereas form 1 remained rather constant after acute activation of the complement system.

Animals↗
PubMed1983

Induction of granulocyte histaminase release by particle-bound complement C3 cleavage products (C3b, C3bi) and IgG.

The interaction of opsonized particles with human granulocytes promotes a number of important biologic functions, including phagocytosis, superoxide generation, and release of a variety of enzymes, including histaminase. We have previously determined that histaminase release occurs via a C3-dependent process. Although fluid-phase C3b dimers can mediate release, the relative effects of particle-bound C3b and C3bi and of IgG have not been examined. In this report we demonstrate that particle-bound C3 deposited on activators of the alternative C pathway effected histaminase release in the absence of IgG. Particle-bound C3bi and C3b were both effective as mediators of histaminase release. The extent of release varied as a function of the activating surface on which C3 was deposited (zymosan C3b was considerably more potent than C3b bound to rabbit erythrocytes, which was slightly more potent than C3b bound to neuraminidase-treated sheep erythrocytes). In contrast, C3b or C3bi deposited on nonactivating surfaces (such as sheep erythrocytes) at inputs of up to 2,000,000 molecules per granulocyte failed to induce histaminase release unless IgG was also present. The ability of C3b bound to particles that serve as activators of the alternative pathway to induce histaminase release is apparently not the result of decreased susceptibility of C3b to proteolysis or to an increased binding affinity to the C3b receptor, but may relate to the interaction of other surface structures on activating particles with the PMN membrane.

Amine Oxidase (Copper-Containing)↗
PubMed1982

Guinea pig erythrocytes, after their contact with influenza virus, acquire the ability to activate the human alternative complement pathway through virus-induced desialation of the cells.

Guinea pig erythrocytes that had been exposed to influenza A virus activated the alternative complement pathway in whole human serum in the absence of natural antibodies. Because all virus particles were eluted from the treated cells, activation was not dependent on antiviral antibodies or on virus particles themselves. The relative capacity of treated erythrocytes to activate the alternative pathway was dependent on the amount of virus to which the cells had been exposed and was directly related to the amount of sialic acid removed from the erythrocyte membrane during incubation with either whole virus particles or purified viral sialidase. C3b bound to cells that had been treated with virus, and P-stabilized amplification convertase sites P,C3b,Bb formed on these cells, exhibited increased resistance to the action of the regulatory proteins beta-1H and C3b Ina compared with C3b and P,C3b,Bb on untreated, nonactivating cells. The acquired resistance of the cell-bound, P-stabilized amplification convertase to decay-dissociation by beta-1H was directly related to the activating capacity of the treated cells in whole serum (r = 0.95) and to the amount of sialic acid removed from the cells by the virus (r = 0.98). Desialation represents a specific alteration of the cell surface by which a nonimmune host, through activation of the alternative pathway, may deposit C3b on a target cell that had been exposed to influenza virus and may lyse virus virus-modified cells during orthomyxovirus infections.

Animals↗