Biomedical subjects

H Owaki

Publications and source records attributed to H Owaki.

28 records · Page 2Linked to original sources

PubMed1989

[Repair of rabbit articular surfaces with allografts of chondrocytes embedded in collagen gels].

In an attempt to restore articular cartilage, allogeneic articular chondrocytes embedded in collagen gels were transplanted onto full-thickness defects in rabbit articular cartilage. Within 24 weeks after the transplantation, the defects were filled with hyaline cartilage, specifically synthesizing type II collagen. These chondrocytes were autoradiographically proven to be originated from the originally transplanted chondrocytes. As histologically assessed, success rate was about 80%, a marked improvement over the results (40% success rate) in previous studies reporting chondrocyte transplantation without collagen gels. On the other hand, the defects without chondrocyte transplantation healed with fibrocartilaginous tissue more than 24 weeks after treatment. Immunological enhancement induced by transplanted allogeneic chondrocytes or collagen was not significant for eight weeks after treatment, so far as shown by both direct and indirect blastformation reactions. Thus, allogeneic transplantation of isolated chondrocytes embedded in collagen gels appears to be one of the most promising methods for the restoration of articular cartilage.

Animals↗

PubMed1988

The presence of a myeloid cell population showing strong reactivity with monoclonal antibody directed to difucosyl type 2 chain in epiphyseal bone marrow adjacent to joints affected with rheumatoid arthritis (RA) and its absence in the corresponding normal and non-RA bone marrow.

The presence of a specific type of cell, highly expressing difucosyl type 2 chain (dimeric Lex; FH-4 antigen), was found in the epiphyseal bone marrow cells of affected joints from patients with active severe rheumatoid arthritis (RA). The antigen was defined by monoclonal antibody FH-4 which was previously found to be directed to the oncofetal marker. The FH-4(+) cell population was identified as myeloid cell lineage with usual morphology specifically found in bone marrow of patients with severe RA, but is virtually absent in the same cell fraction of patients with osteoarthritis, infectious arthritis, and from normal adult subjects.

Adult↗

PubMed1987

A B cell-specific differentiation antigen, CD23, is a receptor for IgE (Fc epsilon R) on lymphocytes.

Two independent L cell transformants expressing human lymphocyte Fc epsilon R were established by using cellular DNA from RPMI 8866 cells. The surface expression of the receptor was confirmed on the basis of the binding of a panel of anti-Fc epsilon R antibodies and its ability to bind IgE. Anti-CD23 antibodies strongly stained the transformants, indicating possible identity or antigenic relationship between Fc epsilon R and CD23. This interesting observation warrants additional clarification as to the role of CD23 and Fc epsilon R in B cell differentiation.

Animals↗

PubMed1986

Molecular structure of human lymphocyte receptor for immunoglobulin E.

We have isolated and sequenced a cDNA clone encoding the human lymphocyte receptor for IgE (Fc epsilon R). The deduced protein sequence reveals that Fc epsilon R consists of 321 amino acids, without any signal sequence, and is oriented with its N-terminus on the cytoplasmic side and its C-terminus on the outside of the cell. This molecule shows striking sequence homology with chicken asialoglycoprotein receptor (hepatic lectin), suggesting a possible role for Fc epsilon R in endocytosis. Fc epsilon R mRNA is expressed in B cells, B cell lines, and macrophage cell lines. It is not expressed in T cells or T cell lines, with the exception of an HTLV-transformed T cell line. mRNAs expressed in a macrophage line and in the latter T cell line differ in size from mRNA expressed in B cells. Human BSF-1 (or IL-4) induces the expression of Fc epsilon R mRNA in B cells, but not in T cells.

Amino Acid Sequence↗

PubMed1986

Fc epsilon receptor, a specific differentiation marker transiently expressed on mature B cells before isotype switching.

The expression of Fc epsilon R on human lymphocytes was studied with the anti-Fc epsilon R mAbs. Fc epsilon R was expressed on most mu+,delta+ circulating B cells, whereas T cells did not express Fc epsilon R even in patients with hyper-IgE syndrome. B cells with gamma, alpha, or epsilon phenotype did not express Fc epsilon R, moreover its expression could not be induced, suggesting that the Fc epsilon R expression was correlated with isotype switching. mu+delta+ B cells in bone marrow did not express Fc epsilon R, but PHA-sup (supernatant from PHA-stimulated cell cultures) could induce its expression, and the addition of IgE augmented this induction. Recombinant IL-2, IL-1, IFN-gamma or -beta, or purified B cell differentiation factor (BSF-2 B cell-stimulatory factor 2) could not induce Fc epsilon R expression in bone marrow B cells. IFN-gamma inhibited the Fc epsilon R expression induced by PHA-sup, suggesting that the human counterpart of BSF-1 may be responsible for Fc epsilon R expression in bone marrow B cells. B cells from patients with common variable immunodeficiency and ataxia telangiectasia did not express Fc epsilon R, but PHA-sup could induce its expression, indicating that circulating B cells of these patients are at a differentiation stage similar to B cells in bone marrow. The study showed that Fc epsilon R is a B cell-specific differentiation marker, the expression of which is restricted to a defined stage of B cell differentiation.

B-Lymphocytes↗

PubMed1986

Monoclonal anti-Fc epsilon receptor antibodies with different specificities and studies on the expression of Fc epsilon receptors on human B and T cells.

Three monoclonal antibodies, 1-7 (gamma 2b), 3-5 (gamma 1), and 8-30 (mu), specific to Fc epsilon receptors (Fc epsilon R) on human B cells were established. The two monoclonals (1-7 and 8-30) could inhibit the binding of IgE to Fc epsilon R in rosette formation assays, as well as FACS analysis, and were shown to recognize the same epitope of Fc epsilon R. The other monoclonal antibody (3-5) recognized the same molecule but a different epitope, and marginally inhibited the IgE binding. The molecules on RPMI 8866 cells recognized by these monoclonal antibodies had Mr of 46,000 and 25,000 to 30,000 daltons as determined by immunoprecipitation and SDS-PAGE analysis. By employing these monoclonal antibodies, the expression of Fc epsilon R on circulating lymphocytes was studied. Approximately 50% of B cells from normal, nonatopic individuals were found to express Fc epsilon R, and a remarkable increase in the expression of Fc epsilon R was observed in B cells of atopic patients. The expression of Fc epsilon R was not detected in T cells from atopic patients (including hyper IgE syndrome) as well as normal individuals. Incubation of B cells with PHA-conditioned medium plus IgE augmented the expression of Fc epsilon R in the Fc epsilon R+ B cell population but not in Fc epsilon R- population. PHA-conditioned medium plus IgE did not induce Fc epsilon R expression on T cells.

Antibodies, Monoclonal↗

PubMed1968