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PubMed2004

Hereditary and acquired angioedema: experience with patients in Puerto Rico.

Hereditary (HAE) and acquired (AAE) angioedema are vascular reactions involving the sub mucosal tissues, representing localized edema caused by dilatation and increased permeability of the capillaries. HAE and AAE are clinical disorders characterized by angioedema that require prompt differentiation from other causes of angioedema in order to receive the most pertinent and effective therapeutic interventions. The aim of this report is to describe the clinical characteristics of patients with both HAE and AAE identified and followed at the Immunology Clinic of the University Hospital at the Puerto Rico Medical Center, their response and side effects to danazol therapy and their comparison with other series of similar patients reported in the literature. Overall, the patients in this sample presented a similar clinical profile compared to other reported series in the literature.

Adolescent↗
PubMed1979

Evidence against the presence of circulating immune complexes in chronic inflammatory bowel disease.

Several investigators have reported the presence of circulating immune complexes in serum from patients with Crohn's disease and chronic ulcerative colitis. Because previous assays employed conditions which might have caused immunoglobulin aggregates to form in vitro, thus falsely suggesting the presence of immune complexes in vivo, we tested inflammatory bowel disease sera for immune complexes using four assays designed to minimize in vitro immunoglobulin aggregation. In three assays immune complexes were not detectable, while in a fourth, the Clq precipitin test, positive reactions occurred. These precipitin reactions did not have characteristics of immune complexes. Our data suggest that circulating immune complexes are either not present in patients with inflammatory bowel disease or that they occur infrequently or in low concentration.

Antigen-Antibody Complex↗
PubMed1979

Levamisole treatment of inflammatory acne. Restoration of impaired T-cell function accompanied by clearing of the lesions.

Serum hemolytic complement activity and its components C3, C4 and C1q, serum immunoglobulins A, M and G and peripheral E-rosette forming cells were determined in 11 patients with inflammatory acne. IgG levels were increased and the E-rosette formation was markedly impaired. Levamisole treatment restored the E-rosette formation and improved or cured the inflammatory lesions in 10 out of 11 patients.

Acne Vulgaris↗
PubMed1991

High doses of intravenous immunoglobulin do not affect the recognition phase of the classical complement pathway.

We have recently found that intravenous immunoglobulin (IVIg) prevents deposition of C3 and C4 fragments onto antibody sensitized erythrocytes. To find out if such an effect results from the blockade of the recognition phase of the classical complement cascade, we investigated the ability of human serum containing high concentrations of IVIg to deposit the recognition subunit of the first complement component (C1q) onto targets. Normal human serum supplemented in vitro with IVIg did not demonstrate reduced C1q binding to targets as determined by radiolabeled antihuman C1q antibody uptake. Similarly, methylamine-treated normal human serum to which IVIg was added was equally effective in terms of C1q binding as the same serum without IVIg. At increasing doses of sensitizing antibody, C1q uptake decreased proportionally; however, at all antibody dilution points C1q uptake was not significantly different in the serum with IVIg in comparison with normal serum. Serum from a patient treated with IVIg did not differ in its capacity to deposit C1q from the same patient's serum before therapy. Our data suggest that IVIg does not interfere with the recognition step of classical complement pathway. This is a US government work. There are no restrictions on its use.

Complement C1↗
PubMed1977

Effect of concanavalin A on the killing of tumor cells by antibody and complement.

Concanavalin A (Con A) was found to inhibit the killing of antibody-sensitized line-1 tumor cells (TA) by guinea pig complement (GPC) but not by human complement (HuC). Other plant lectins (wheat germ, leucoagglutinin, and pokeweed mitogen) were also tested but Con A was the only lectin found to inhibit antibody-GPC-mediated killing. The inhibitory effect of Con A was observed when the GPC was mixed with Con A or when the antibody-sensitized cells were pretreated with Con A (TA-Con A) before the addition of GPC. The effect could be reversed by treatment of such cells with alpha-D-methylglucopyranoside or by incubation at 37 degrees C for approximately 2 hr. Con A appeared to act by preventing the binding of the first component of GPC (GPC1) to antibody-sensitized tumor cells. Differences in the binding of the first component of HuC (HuC1) and GPC1 to TA-Con A suggested that a difference in the binding site for HuC1 and GPC1 might exist. There was no difference in the number of GPC1 molecules fixed to antibody-sensitized sheep erythrocytes (EA) or EA treated with Con A in experiments using the same antibody as used with the tumor cells and the same Con A preparation. It would consequently appear that the inhibitory effect of Con A on the binding of GPC1 to TA is not due solely to an interaction of Con A with the antibody.

Animals↗
PubMed1977

Tissue localization of C1q in HBs antigen positive liver disease patients by direct immunofluorescent technique.

Tissue localization of a subcomponent of the first component of complement (CLq) was examined in one postmortem case of HBs antigen (HBs Ag) positive hepatocellular carcinoma and in six cases of chronic hepatitis from liver biopsy specimens. The direct immunofluorescent method was used after fixation with 2% para-formaldehyde in concentrated ammonium sulfate. CLq localization was found in collagen fibers and the cytoplasm of fibroblasts in the connective tissues of specimens examined. The localization was particularly marked in the region of the fundal glands of the gastric wall. Apart from collagen fibers, other sites of localization included the surface membrane of lymphocytes, especially those cells of the mesenteric lymph nodes. In HBs Ag positive specimens, immune deposit-like substances appeared localized intra-hepatically and in the renal glomeruli. Since C3 and C4 were identified concomitantly, it indicates that these substances were indeed immune diposits. Despite the finding that C3 and C4 were identified together in the hepatic cell cytoplasm, C1q itself was not demonstrated in all hepatic cell cytoplasms.

Carcinoma, Hepatocellular↗
PubMed1977

Separation of hydroxyproline-containing protein from C1q (a subcomponent of complement) in serum.

Precipitation of the euglobulin fraction from serum separates C1q from another hydroxyproline-containing protein(s), which remains in the serum-minus-euglobulin fraction. The presence of C1q in the euglobulin fraction has been verified by radial immunodiffusion assay, by sensitivity to collagenase, by hydroxyproline content, and by electrofocusing. The presence of another hydroxyproline-containing protein(s) in the serum-minus-euglobulin fraction has been verified by the same criteria. The isoelectric pH range of C1q is 6.1-7.0; the isoelectric pH range of the other hydroxyproline-containing protein(s) is 4.2-5.5.

Blood Protein Electrophoresis↗
PubMed1991

Antilymphocytic antibodies and marrow transplantation. XIV. Antibody-induced suppression of graft-versus-host disease in C3-decomplemented mice differentiates two T-cell-depletion pathways.

Remarkable differences in the suppression of graft-versus-host disease (GVHD) have been found for anti-Thy-1 antibodies to relate to (1) antigen density and antibody coating on the target cells, (2) antibody isotype, and (3) uptake of complement subcomponent C1q. Regarding (2) and (3) we now demonstrate that depletion of the third complement component C3 by cobra venom factor (CVF) differentiates two T-cell elimination pathways in mice: four rat IgG2c anti-Thy-1 monoclonal antibodies (MoAbs) with low uptake of mouse C1q lost most of their T-cell-depleting and consequently GVHD-preventing effect in C3-depleted H2 IA incompatible semiallogeneic (C57BL/6xCBA)F1 mice. In contrast, eight rat IgG2b, mouse IgG2a, and 2b anti-Thy-1 MoAbs with high affinity for C1q still remained strongly T-cell-depleting and prevented GVHD even in fully mismatched CBA mice depleted of C3. In conjunction with our observation that anti-Thy-1 MoAbs also suppress GVHD in C5-deficient AKR mice, we conclude that complete complement activation until T-cell lysis is not required for our antibodies to be effective in vivo. Activation, but only until deposition of C3b on target-cells for opsonisation via C3b receptors, is necessary with the less immunosuppressive anti-Thy-1 IgG2c isotype with low affinity for C1q. Mouse C1q uptake and C3/C4 deposition on target cells were measured with labeled antibodies and localized in T-cell areas. Interestingly, not even activation until C3b is necessary with the most immunosuppressive C1q-high-affine isotypes. As far as the latter is concerned, we discuss whether elimination of antibody-coated cells via Fc receptors is enhanced by binding to C1q-receptors and/or by intercalating C1q expressed on macrophages.

Animals↗
PubMed1978

Circulating immune complexes in African mothers and their newborns.

Circulating immune complexes were measured using the Clq-binding test in 185 African mothers and their newborns at delivery. Results were compared to non-pregnant African women, healthy European blood donors and to a group of European mothers and their newborns. Clq-binding activity was increased in African mothers and in non-pregnant African women. Circulating immune complexes rarely occurred in cord blood even when mothers showed a high Clq-binding activity. The levels of immune complexes were unrelated to malaria. Complement components Clq and C3 were lower in the newborns than in the mothers.

Antigen-Antibody Complex↗
PubMed1986

Interaction of C1q subcomponent with immunoglobulin M.

The affinity of human C1q subcomponent for IgM of normal human serum and Waldenström macroglobulins of patients Sew and Zuk were investigated by the polyethylene glycol 6,000 immune complexes precipitation test. This test was calibrated with heat-aggregated gamma-globulin (HAGG); maximum fixation of C1q ranged from 60 to 80% (measured as percentage of radioactivity of the immune complexes precipitate) and was observed when the C1q:HAGG concentration ratio was about 1:250. At the ratio of 1:20 the radioactivity of the precipitate was about 43% of the total. The capacity of polyclonal IgM and Waldenström macroglobulins for C1q fixation is low and variable. The percentage of C1q fixed at the C1q:IgM ratio of 1:20 for polyclonal IgM and Zuk macroglobulin was about 9%, whereas for Sew it was only about 1%.

Complement Activating Enzymes↗
PubMed1987

Presence of fucolipid antigens with mono- and dimeric X determinant (Lex) in the circulating immune complexes of patients with adenocarcinoma.

A series of fucosylated glycosphingolipids with the Lewisx (Lex) determinant (Gal beta 1----4[Fuc alpha 1----3]GlcNAc) have been shown to accumulate in human adenocarcinomas. Lex glycolipids were eluted from Protein A-silica columns over which plasma from patients with adenocarcinoma had previously been perfused. The fact that Protein A has strong affinity for IgG and IgG-immune complexes suggested that the Lex antigens isolated from Protein A eluates were complexed with IgG. Lewisx antigen eluted from Protein A columns banded in the immune complex-enriched region (below IgG) of neutral sucrose density gradients. A modified Raji cell assay and an anticomplement C1q enzyme-linked immunosorbent assay were also used for measurement of Lex antigen associated with C3- and C1q-CIC, respectively. Following affinity purification of Lex-IgG complexes and subsequent dissociation of these immune complexes, human antibodies were isolated which reacted with purified glycosphingolipids containing Lex. Levels of Lex-IgG complexes were found to be 2- to 5-fold higher in eluates of Protein A-silica columns perfused with plasma from adenocarcinoma patients compared to eluates from columns perfused with plasma from healthy individuals and patients with other cancers. These assays may prove to be of diagnostic and/or prognostic significance in adenocarcinoma.

Adenocarcinoma↗
PubMed1988

Selective synthesis of mRNA and proteins by human peripheral blood neutrophils.

Human peripheral blood polymorphonuclear neutrophils (PMN) have been considered to be capable of little if any protein biosynthesis. We evaluated the ability of PMN to synthesize both mRNA and proteins. Using in vitro [35S]methionine pulse-chase labeling of purified PMN, followed by immunoprecipitation of cell lysates with immobilized mAb and analysis by gel electrophoresis, PMN were shown to synthesize CR1, FcR, CR3 alpha-chain, MHC class I, and actin. In contrast, incorporation of [35S]methionine into either CR3 beta-chain or the secondary granule protein lactoferrin was not detected. Purification of mRNA from PMN and analysis by Northern blots demonstrated the presence in PMN of CR1, actin, and MHC class I transcripts. However, despite the apparent lack of CR3 beta-chain biosynthesis, specific beta-chain message was detectable in PMN RNA. Inhibition of mRNA synthesis in PMN with actinomycin D resulted in decreased synthesis of nascent CR1, FcR, MHC class I, and actin compared with control cells. Thus, PMN continue to transcribe and translate the genes for certain membrane and cytoskeletal proteins. In contrast, the lack of detectable synthesis of either lactoferrin or CR3 beta-chain suggested that biosynthesis in circulating PMN is selective.

Blood Proteins↗