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At least 1,603 records · Page 89Linked to original sources
PubMed1978

Autoimmunity in psoriasis. Relation of disease activity and forms of psoriasis to immunofluorescence findings.

Immunofluorescence (IF) studies using the test providing information on the reactivity of stratum corneum (SC) antibodies and their in vivo binding have been performed in 193 cases of psoriasis and 89 cases with other dermatoses. It has been shown that: 1. Essentially all fully developed, active psoriatic lesions had IgG deposits in the stratum corneum at the sites of the SC antigen, presumably due to in vivo binding of SC antibodies. 2. In various forms of psoriasis SC antigen sites appeared to be completely or almost completely satured with in vivo deposits of IgG as seen in tests with SC antibodies. 3. In most but not all lesions complement components C3 and/or C4 was found in a comparable pattern in the SC, especially when multiple specimens of single cases were studied. Partial or complete saturation of the SC antigen could be observed by the performance of complement indirect IF tests for SC antibodies in such specimens. 4. In lesions with typical histology of psoriasis the above-mentioned immunologic characteristics appeared to be a constant finding. However, in specimens of recent lesions which had not yet developed typical histology a proportion (2 of 17) were negative both for IgG and complement deposits. In receding lesions weak deposits of IgG were present only in a few specimens and complement deposits were as a rule negative. 5. In a group of 89 control specimens of other dermatoses only occasional cases gave the psoriasiform IF pattern, but about 30% of the specimens gave positive reactions in the SC though these were usually of a different pattern.

Antibody Formation↗
PubMed1978

Chemotactic effects of the complement-derived peptides C3a, C3ai and C5a (classical anaphylatoxin) on rabbit and guinea-pig polymorphonuclear leukocytes.

The complement-derived peptides C3a, C3ai and C5a (= classical anaphylatoxin) were purified from hog serum and examined for chemotactic activity on rabbit and guinea-pig polymorphonuclear leukocytes (PMN) with the Boyden chamber technique (with filters of 3,0 micrometer pore size). When media containing albumin or serum were used all peptides induced chemotaxis of both cell species. Only C3a showed a pronounced species dependence in that it was much more active on rabbit than on guinea-pig PMN. No gross differences were found between the influence of 0.5% BSA and 10% heated (56 degree, 30 min) homologous serum added to the medium. In the absence of protein chemotaxis did not occur.

Anaphylatoxins↗
PubMed1981

Suppression of human lymphocyte migration by PGE2.

Prostaglandin (PG) E2 markedly inhibits casein- and C5a-stimulated lymphocyte migration in a concentration-dependent manner. Inhibition is observed with as low as 10(-9) M PGE2 and requires that PGE2 be present during cell locomotion. Studies with PGE1, PGF1 alpha, PGF2 alpha and PGA1 indicate that only PGE1 and PGE2 inhibit lymphocyte migration. These studies indicate that PGE2 may play a role in the regulation of the immune response at the level of lymphocyte locomotion.

Caseins↗
PubMed1980

Digital integration of granulocyte aggregation responses. A simple and reproducible method for the quantitation of granulocyte adhesiveness.

The pulmonary leukostasis and lung dysfunction associated with intravascular complement activation results from C5a-mediated granulocyte (GR) aggregation, a phenomenon which can be reproduced in vitro using standard nephelometric techniques. To produce a more subjective measure of the extent and rate of GR aggregation responses we added a digital integrator to the system. The validity of this approach was substantiated by the close correlation between the aggregating and chemotactic activities of C5a and N-formyl-methionine-leucine-phenylalanine. Use of this technique enabled us to define the dose-response relationship of the aggregation produced by the cationophore A23187 and the inhibitory effect of tetracaine on divalent cation-dependent aggregation responses. The aggregation produced by these three stimuli does not result primarily from simple cross-linking of surface changes because, unlike the passive cell-cell association produced by the cation poly-L-lysine, it is not inhibited by anionic poly-L-glutamic acid. The importance of microtubules as regulators of GR adhesiveness was substantiated by the inhibitory effects of colchicine (but not lumicolchicine) on aggregation in this system. These data suggest that this integration of light transmission increments is a useful adjunct to this basic technique, whether used as a bioassay for chemotactic stimuli or as a model to study the many factors which regulate GR adhesiveness.

Calcimycin↗
PubMed1984

Experimental monoarthritis. Modulatory effect of injected eosinophils on influx of various types of inflammatory cells.

Bovine serum albumin (BSA) in complete Freund's adjuvant (CFA) was injected into the knee joints of previously BSA-sensitized guinea pigs and rabbits. The primary immune reaction to BSA prevented secondary immune response to Trichinella larvae infection. We were unable to produce either eosinophilia in the peripheral blood or antibodies against Trichinella antigen (shown by complement fixation test). The additional injection of mediators of the inflammatory reaction or their precursors, e.g., complement component C5 and arachidonic acid, caused different histological pictures. C5 produced a prolonged acute inflammatory phase with abundant neutrophils, whereas arachidonic acid did not significantly change the inflammatory response as compared to controls. The additional application of eosinophil-enriched preparation (EEP) caused a conspicuously reduced influx of monocytes/macrophages, a reduction of lymphocyte numbers, a prolonged influx of neutrophils, increased arylsulfatase activity, earlier reduction of the inflammatory process, and earlier onset of synoviocyte regeneration as compared to controls.

Animals↗
PubMed1984

Ibuprofen inhibits granulocyte responses to inflammatory mediators. A proposed mechanism for reduction of experimental myocardial infarct size.

The use of nonsteroidal antiinflammatory agents to reduce myocardial infarct size has demonstrated a dichotomy between ibuprofen, which reduces myocardial infarct size, and aspirin, which does not. A feline model of coronary ischemia using ligation of the anterior descending artery demonstrated that intravenous ibuprofen (2.5-20 mg/kg) given immediately and 2 h after ligation significantly decreased (by about 40%) myocardial infarct size. In contrast, aspirin did not diminish infarct size at any achieved dose; in fact, at some doses it tended to increase infarct size. In vitro studies with purified granulocytes demonstrated a similar dichotomy between ibuprofen and aspirin. Ibuprofen inhibits granulocyte aggregation, superoxide production, lysosomal enzyme release, and granulocyte-mediated endothelial cytotoxicity, while aspirin is without effect on these modalities. We propose that ibuprofen's beneficial effect in experimental myocardial ischemia is related to its ability to inhibit activated granulocytes and thus to diminish myocardial cell death in experimental myocardial infarction.

Animals↗
PubMed1999

T-cell receptor vbeta deletion and valpha polymorphism are responsible for the resistance of SWR mouse to arthritis induction.

Collagen type II-induced arthritis (CIA) develops in susceptible mouse strains after intradermal injections of type II collagen (CII) in complete Freund's adjuvant (CFA). Susceptibility to CIA in mice is linked to genes of the major histocompatibility complex (MHC). Although the SWR mouse has a susceptible MHC haplotype (H2q), it is resistant to CIA. SWR exhibits at least two known immunological defects: (1) it contains a germline deletion of about 50% of T-cell receptor (TCR) Vbeta-chain gene segments, and (2) SWR is deficient in complement component C5. It has been shown that T cells that express TCRValpha11.1 and TCRVbeta8.2 play a substantial role in the pathogenesis of arthritis in the DBA/1 mouse (H2q). We generated SWR transgenic (tg) mice to determine whether the expression of pathogenic Valpha11.1 and/or Vbeta8.2 transgenes would confer arthritis susceptibility. Arthritis was induced in the SWR TCRalphabeta tg mice, but not in SWR TCRbeta tg mice. To address the role of Valpha11.1 in arthritis susceptibility, we examined the allelic polymorphisms of the Tcra-V11-gene subfamily members between the arthritis susceptible DBA/1 mouse and the arthritis-resistant SWR mouse strain. The amino acid sequences of the Valpha11.1 alleles differ at two positions (codons 18 and 68). Accordingly, these two amino acid changes are sufficient to allow the production of pathogenic T cells in SWR mice. This is the first demonstration of the association of a particular Tcra-V allele and arthritis susceptibility in mice.

Animals↗
PubMed2003

The KRN mouse model of inflammatory arthritis.

In 1996 a new murine model of spontaneous arthritis was described by the group of Benoist and Mathis. Mice transgenic for a T cell receptor recognizing an epitope of bovine RNase and bred onto a NOD background developed severe destructive arthritis, which resembles human rheumatoid arthritis in many respects. The development of disease requires the presence of T and B lymphocytes and is dependent on the MHC class II molecule I-A(g7). B cell activation by antigen and an additional CD40-CD40 ligand interaction was found to give rise to the production of autoantibodies. Glucose-6-phosphate isomerase was identified as the target of the autoantibodies; moreover, the transgenic T cells were demonstrated to exhibit a dual specificity for both bovine RNase and glucose-6-phosphate isomerase. Importantly, the arthritis is serum transferable to normal recipients, enabling the examination of the pathogenic mechanisms of joint inflammation and destruction. Recent studies suggest the crucial involvement of the innate immune system in the development of antibody-induced arthritis. Complement components, Fc receptors and neutrophils are indispensable for disease induction. An overview of the existing data is given and the emerging concepts of the pathogenesis of the K/BxN arthritis are discussed with respect to their relevance for human rheumatoid arthritis. Because of the reliable and robust induction of joint inflammation by serum transfer this new disease model has been and will be a valuable means to address the as-yet-unanswered key questions related to the development of arthritis.

Animals↗
PubMed1980

Immunosympathectomy: lack of evidence for a complement-mediated cytotoxic mechanism.

To determine whether the destruction of peripheral sympathetic neurons by anti-NGF-antibodies results from a complement-mediated cytotoxic action or from the deprivation of endogenous NGF or immunologically NGF-like cross-reacting molecules we investigated the time-course of the reversibility of the effect of NGF-antibodies by neutralizing doses of NGF, together with the effect of NGF-antibodies in complement-deficient mice. After administration of a single dose of 50 mg/kg of purified antibodies to newborn rats the TH level was reduced to 75% of controls after 12 h, to 48% after 24 h, 39% after 36, and 28% after 48 h. After this time no further reduction occurred and levels remained constant up to 14 days. The effect of the NGF-antibodies was reversible on addition of NGF up to 48 h after antibody administration. Although the reversibility was not complete (85% of controls) the extent of the reversibility was the same whether NGF was given 12 or 48 h after the antibodies. The incompleteness of the reversibility is reflected by the small number of degenerating neurons apparent as early as 12 h after antibody administration. Since these early degenerative effects were also seen in complement-deficient mice it is concluded that they involve a small population of neurons, sensitive to short-term NGF deprivation whereas the majority of the neurons can withstand deprivation for up to 48 h without sustaining irreversible damage.

Adrenergic Fibers↗
PubMed1984

Effect of indomethacin on generation of chemotactic activity in inflammatory exudates induced by carrageenan.

Chemotactic activity of protein origin was demonstrated in carrageenan-induced pleural exudates by the chemotactic response of neutrophils in the modified Boyden chamber. The activity was partly neutralized by monospecific antisera to complement component 5 and was destroyed by trypsin and chymotrypsin treatment but it differed from that in rat serum or plasma in that it was stable for 30 min at 56 degrees C. Indomethacin (5 mg/kg i.v.) reduced equally protein content (56%) and total chemotactic activity (58%); i.e., chemotactic activity/mg of exudate protein was unchanged. Intrapleural injection of autologous or homologous serum also induced an infiltration of neutrophils; the protein content of the pleural fluid decreased by 60-70% in 4 h, whereas with carrageenan there was a progressive increase in exudate protein. When serum was injected in two doses to maintain protein levels comparable to those found following carrageenan injection, the number of neutrophils in the exudates was also comparable. In contrast to carrageenan, the response to serum was not inhibited by indomethacin. From these and other data we suggest that the exudate chemotactic activity is generated from plasma protein and that indomethacin acts primarily to reduce extravasation of plasma and consequently generation of chemotactic activity.

Animals↗
PubMed1980

A 48-well micro chemotaxis assembly for rapid and accurate measurement of leukocyte migration.

We designed a 48-well chemotaxis chamber to minimize manipulation time and amount of material required by the larger blindwell or Boyden chemotaxis chamber. Cell and chemoattractant dose-response curves showed that results were comparable to our better than those obtained with blindwell chambers. The volume of chemoattractant per well is 25 microliter; the number of cells can be as low as 10,000. The time needed for setting up this multiwell unit and for staining the membrane filter sheet is negligible. Combined with the use of an image analyzer to count the number of migrated cells, the method is suitable for clinical research on the functional state of monocytes in large groups of patients.

Chemotactic Factors↗