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Biomedical subjects

C G Kallenberg

Publications and source records attributed to C G Kallenberg.

264 records · Page 15Linked to original sources
PubMed1980

Systemic involvement and immunologic findings in patients presenting with Raynaud's phenomenon.

Systemic involvement and spectrum of autoantibodies were evaluated in 91 patients presenting with Raynaud's phenomenon. Decreased pulmonary diffusing capacity was observed in 23 percent, esophageal hypomotility in 14 percent and renal involvement in 5 percent of the patients, all without clinical symptoms. Arthralgia or a history of arthritis was present in 27 percent and skin abnormalities in 30 percent. Extent of systemic involvement was correlated with the severity of Raynaud's phenomenon, as measured by photoelectric plethysmography (r = 0.38; p < 0.01). In addition, both the variety of different autoantibodies in the serum of individual patients and the titer of antinuclear antibodies were positively correlated with the number of affected organ systems (r = 0.63; p < 0.01 and r = 0.65; p < 0.01, respectively). Raynaud's phenomenon is an important clinical sign of asymptomatic systemic disease. Measurements of its severity and serologic parameters are helpful in predicting the extent of systemic involvement.

Adult↗
PubMed1980

Defective stimulating capacity of leukocytes in mixed leukocyte culture in constitutional aplastic anemia caused by suppressor T cells. A case study.

A patient with constitutional Fanconi-like aplastic anemia who developed a preleukemic state was transplanted with bone marrow from his HLA-identical MLC-negative brother. Before transplantation his mononuclear leukocytes were found to have a defective stimulating and responder capacity in mixed leukocyte culture with cells of an unrelated individual. After removal of T cells the stimulating capacity was completely restored. MLC testing with separated cell fractions seems important to establish HLA-D identity with a possible donor, especially when MLC tests with unseparated cells are negative.

Adult↗
PubMed1980

Suppression of DNA synthesis by con A-activated human lymphocytes: role of monocytes in con A-induced suppression.

Human peripheral blood mononuclear leucocytes, activated by Con A, suppress the antigen- or mitogen-induced proliferation of autologous responder cells. Generation of suppressor cells is prevented by mitomycin treatment before Con A activation. Once cells are activated, their suppressive activity is not affected by mitomycin treatment. Monocytes are not only required for generation of suppressor cells, but are also involved in suppression as effector cells. Monocyte-mediated suppression is blocked by indomethacin, suggesting that this suppression is mediated by prostaglandin. It is concluded that monocytes are involved in Con A-induced suppression of DNA synthesis.

Cell Division↗
PubMedDate not supplied

In vitro up-regulation of E-selectin and induction of interleukin-6 in endothelial cells by autoantibodies in Wegener's granulomatosis and microscopic polyangiitis.

OBJECTIVE: In patients with Wegener's granulomatosis (WG) or microscopic polyangiitis (MPA) autoantibodies to myeloid granule proteins (ANCA), particularly proteinase 3 (Pr3) and myeloperoxidase (MPO), and to endothelial cells (AECA) are frequently detected. The role of these autoantibodies in the development of vascular injury is incompletely understood. Since the expression of E-selectin and the production of interleukin 6 by endothelial cells is an early step in the sequence of events leading to vascular injury, we examined the capacity of IgG fractions from patients with WG and/or MPA to activate endothelial cells to the expression of E-selectin and the production of IL-6. We related those findings to the presence of ANCA and AECA in the IgG preparations. METHODS: Human umbilical vein endothelial cells (HUVEC) were incubated with immunoglobulin (IgG) preparations from 28 patients (17 positive for anti-Pr3, 10 for anti-MPO, and one for anti-Pr3/MPO) with active vasculitis and from 10 healthy volunteers. The final IgG concentration in the activation assay was 2 mg/ml. TNF alpha (10 ng/ml) and LPS (10 ng/ml) were used as positive controls for HUVEC activation. The extent of HUVEC activation was assessed by the measurement of E-selectin expression by flow cytometry (after 4 hours of incubation) and the production of interleukin 6 by ELISA (after 24 hours). RESULTS: We found that 11 of the 28 ANCA positive IgG samples were capable of activating endothelial cells: six samples induced IL-6 production alone, one sample upregulated E-selectin expression alone, and four samples induced both IL-6 production and E-selectin upregulation. Five of 17 anti-Pr3 positive samples (one of which was also positive for AECA) and 6 of 10 anti-MPO positive samples (all simultaneously positive for AECA) induced endothelial cell activation. AECA positive samples that induced endothelial cell activation (n = 7) had higher AECA titres than samples that did not induce endothelial cell activation (n = 6). CONCLUSION: Our data suggest that the activation of endothelial cells in patients with WG and MPA can be induced by circulating autoantibodies. Both ANCA and AECA can be responsible for this effect.

Adolescent↗
PubMedDate not supplied

Anti-neutrophil cytoplasm autoantibodies (ANCA) in autoimmune liver diseases.

Anti-neutrophil cytoplasm antibodies (ANCA) are autoantibodies directed against cytoplasmic constituents of neutrophil granulocytes and monocytes. ANCA have been detected in serum from patients with inflammatory bowel diseases (mainly ulcerative colitis) and autoimmune mediated liver diseases (mainly primary sclerosing cholangitis and autoimmune hepatitis-type 1). The antigens recognized by ANCA in these diseases are multiple and the clinical and pathophysiological significance of ANCA in these disorders has not been completely defined.

Antibodies, Antineutrophil Cytoplasmic↗
PubMedDate not supplied

Membrane proteinase 3 expression on resting neutrophils as a pathogenic factor in PR3-ANCA-associated vasculitis.

Antineutrophil cytoplasm autoantibody (ANCA)-associated small vessel vasculitides are systemic diseases characterized by chronic inflammation of blood vessels. These vasculitides are associated with the presence of ANCA which are, in most cases, directed towards proteinase 3 (PR3) or myeloperoxidase (MPO). In vitro and in vivo data have suggested a pathophysiological role in the ANCA-associated vasculitides, particularly based on the capacity of autoantibodies to bind and activate neutrophils. This review focuses on the role of constitutive expression of proteinase 3 on the membrane of resting neutrophils (mPR3). mPR3 can be expressed on the total population or on a subset of neutrophils and levels of mPR3 differ between individuals. The level of mPR3 on resting neutrophils and the percentage of mPR3 expressing neutrophils is stable in time for a given individual, suggesting a genetic determinant. Patients with ANCA-associated vasculitis have an increased constitutive expression of mPR3 on resting neutrophils compared to healthy controls. High levels of mPR3 on resting neutrophils are a risk factor for the development of relapses in patients with PR3-ANCA-associated vasculitis, probably by making resting neutrophils more susceptible for binding ANCA and induction of activation. As such, constitutive mPR3 expression on neutrophils seems another pathogenic factor in ANCA-associated vasculitis.

Antibodies, Antineutrophil Cytoplasmic↗
PubMedDate not supplied

Detection of autoantibodies to ribonucleoproteins by counter-immunoelectropheresis, immunoblotting and RNA-immunoprecipitation: comparison of results.

Counterimmunoelectropheresis (CIE), immunoblotting (IB) and RNA-immunoprecipitation (RNA-IP) were compared for their potential to detect antibodies to U1RNP, Sm and SS-B in sera from 50 patients with SLE and 18 with MCTD. Anti-SS-B were detected in 6 SLE-sera (12%) and one MCTD-serum (6%) by all three techniques. Anti-Sm were present in 7 SLE-sera (14%) by RNA-IP and IB; 3 of these sera showed identity with a-Sm and 4 with a-U1RNP by CIE. Antibodies precipitating U1RNA were present in 8 SLE sera (16%); 4 of these sera were positive for anti-U1RNP by CIE (8%) and 4 sera recognized one or more of the U1RNA-associated proteins by IB (8%). All MCTD-sera were positive for anti-U1RNP by RNA-IP including one serum negative by IB and CIE. RNA-IP allowed the detection of antibodies precipitating U1-U2RNA in 4 sera; in IB, the U2RNA specific protein B" was recognized by 3 sera. RNA-IP appears to be a sensitive method for detecting anti-URNP's.

Autoantibodies↗
PubMedDate not supplied

Platelet activation, fibrinolytic activity and circulating immune complexes in Raynaud's phenomenon.

Circulating immune complexes (CIC), platelet activation and fibrinolytic activity were assessed in 133 patients with Raynaud's phenomenon (RP), 41 with primary RP, 73 with secondary RP and 19 with RP and minor symptoms of connective tissue disease (suspected secondary RP). Increased levels of CIC were found in secondary and suspected secondary RP. In those groups spontaneous platelet aggregation also was found, a percentage of which correlated with levels of CIC. In all groups elevated levels of beta-thromboglobulin, a platelet specific protein released during platelet activation, and decreased levels of alpha 2-antiplasmin, the main inhibitor of fibrinolysis, were found, together with hyperfibrinogenemia.

Adult↗