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Biomedical subjects

S M Fu

Publications and source records attributed to S M Fu.

143 records · Page 8Linked to original sources
PubMed1975

A scanning electron microscopy and immunological study of 84 cases of lymphocytic leukaemia and related lymphoproliferative disorders.

The surface features of cells from 84 cases of lymphocytic leukaemia, and related lymphoproliferative disorders are described as seen by scanning electron microscopy (SEM). Most of the 46 cases of CLL were shown to be B-derived, but rare cases of mixed B and T cell leukaemia and leukaemia with cells bearing both B and T markers were also encountered. Despite the existence of a spectrum of cell surface morphology, it was possible in many cases to identify a dominant cell type. Cells from cases of B derived malignancies were most frequently of the 'predominantly villous' type while a smaller proportion of cases were of the predominantly 'smoother' or 'mixed villous and smooth' type. Variations in surface morphology also occurred with progression of the disease. In most cases of acute lymphoblastic leukaemia (ALL) 'smoother' cells predominated. However, more cases of ALL and T derived leukaemia need to be examined before definite conclusions can be drawn concerning the surface of these cell types. This study also illustrates the importance of examining large numbers of cases of leukaemia, before conclusions are drawn concerning their surface features and indicates that SEM cannot consistently distinguish between leukaemic B and T cells. It will be of interest to determine whether the surface architecture of the leukaemic cell is related to the degree of cell differentiation and eventual prognosis in these cases.

B-Lymphocytes↗
PubMed1975

Immunofluorescent studies on antibodies directed to a buried membrane structure present in lymphocytes and erythrocytes.

Brief digestion of human peripheral blood lymphocytes by vibrio cholera neuraminidase (VCN) revealed hidden components of the membrane. Autologous human serums contained antibodies directed to these components that were readily demonstrated by immunofluorescence. Antibodies of similar specificity were found in all normal serums. The antibodies were principally of the IgM variety with lesser amounts of the IgG class present. They were equally active at 4 degrees C and 37 degrees C. The VCN revealed membrane determinants were present in normal B and T lymphocytes, monocytes, lymphocytes of patients with chronic lymphatic leukemia and cells of lymphoid lines. The newly revealed determinants slowly disappeared upon culture of the lymphocytes. These hidden components were similarly demonstrated in erythrocyte membranes and represent the T antigen long known for the red blood cells. Absorption by either VCN treated autologous lymphocytes or erythroyctes removed all of the antibodies capable of reacting with both cell types. Absorption by VCN digested isologous lymphocytes removed all reactivity with autologous lymphocytes.

Absorption↗
PubMed1975

B lymphocytes lacking surface IG in patients with immune deficiency: initiation of IG synthesis in culture in cells of a patient with thymoma.

A 64-year-old woman with a syndrome of thymoma, severe hypogammaglobulinemia, seemingly normal cell-mediated immunity and aplastic anemia, was found to have virtually no immunoglobulin- (Ig) bearing peripheral blood lymphocytes (PBL). However, 7.8 +/- 3.4% of the PBL were positive for another B-cell marker, the receptor for aggregated IgG, while the remaining cells bound sheep erythrocytes. Those cells which were aggregate-reactive appeared to be immature or incomplete B cells. Cultures of peripheral blood leukocytes from the patient in various serum-containing media were studied by 3 independent technics for the development of lymphocyte surface Ig and for Ig in the culture supernatants. In vitro the patient's cells were able to develop surface Ig in media supplemented with fetal calf serum (FCS) or normal serum; in media supplemented with autologous serum, the cells developed no surface Ig. During the cultures in FCS, human Ig determinants became detectable in the medium, and both medium and cell-surface Ig underwent a shift from mu determinants early in the culture period to gamma and alpha determinants later. The development of Ig on the cells was not inhibited by the presence of autologous serum if FCS was included in the medium. These data support the concept that a factor, missing from this patient's serum, is required at an early stage in the maturation of the B cell. A patient with X-linked agammaglobulinemia had a population of circulating lymphocytes with surface characteristics similar to the B cells of the thymoma case. In contrast, no Ig synthesis by this patient's cultured cells could be demonstrated, indicating a different level of block in the 2 cases despite their similarity at the level of the cell surface.

Agammaglobulinemia↗
PubMed1975

Similar idiotypic specificity for the membrane IgD and IgM of human B lymphocytes.

Certain cases of chronic lymphocytic leukemia possess monoclonal bands in the serum. Idiotypic antibodies to the isolated IgM protein of one such case demonstrated that the leukemic lymphocytes carried the identical specificity on their lymphocytes. Both the lymphocyte IgM and the IgD possessed this same specificity. This was demonstrated best through the use of rhodamine-conjugated Fab fragments of IgM- and IgD-specific antisera which were both capped by the idiotypic antiserum.

Animals↗
PubMed1975

IgG on lymphocyte surfaces; technical problems and the significance of a third cell population.

Direct immunofluorescence performed with the F(ab)2 fragment of rabbit antibodies to IgG revealed that membrane bound IgG was only rarely found on the surface of small peripheral blood lymphocytes (PBL). In contrast whole antibodies to IgG used in fluorescence gave much higher levels of cells with IgG surface staining. This staining resulted from secondary IgG binding, in part due to the uptake of newly formed immune complexes. IgM-and IgD-bearing cells were brightly stained in relatively similar percentages by both the whole and F(ab)2 forms of the class-specific antibodies; they constitute the principal membrane Ig of PBL. Evidence was obtained indicating that a special population of cells with Fc receptors but lacking membrane Ig was primarily involved in the high IgG binding. This population also formed sheep erythrocyte rosettes when optimal conditions were utilized.

Animals↗
PubMed1974

Evidence for linkage between HL-A histocompatibility genes and those involved in the synthesis of the second component of complement.

HL-A analysis of a family with C2 deficiency revealed evidence for close linkage between the C2 defect and the histocompatibility HL-A loci. The propositus was homozygous both for C2 deficiency and the HL-A haplotype 10,W18. Among seven children of three double backcross matings, no recombinants were found. The possible significance of such linkage is discussed.

Complement System Proteins↗
PubMed1974

Membrane immunoglobulins of B lymphocytes: inability to detect certain characteristic IgM and IgD antigens.

Hemagglutination and fluorescent antibody studies have provided strong evidence for the unavailability or absence of specific antigenic sites on membrane-bound IgM which are present in serum and intracellular IgM. Antisera specific for different parts of the molecule indicated that a portion but not all of the Fc was involved. Absorption experiments with normal and leukemic viable B lymphocytes failed to remove a population of Fc antibodies found in IgM-specific antisera. Similar findings were made for IgD, the other major membrane immunoglobulin of human peripheral blood B cells. Various interpretations of these observations are discussed. The most likely possibility appears that the C-terminal portion of the heavy chains of the immunoglobulin molecule is buried in the membrane.

Antibodies, Anti-Idiotypic↗
PubMed1974

Scanning electron microscopy of human lymphocyte-sheep erythrocyte rosettes.

Human lymphocytes of known B or T derivation were examined by scanning electron microscopy (SEM) before and after rosetting with SRBC. After collection of the cells onto silver membranes the samples were prepared for SEM by the critical point drying method. Sheep RBC frequently underwent sphero-echinocyte transformation and multiple projections extended from their surfaces. This was readily noticeable after storage of SRBC in the cold and washing in Hanks, but more prominent after rosetting. These erythrocyte surface alterations were less apparent when freshly withdrawn cells were used. Spontaneous sheep erythrocyte rosettes (E-R), a marker for human T lymphocytes, were prepared with normal peripheral blood lymphocytes (PBL), thymic cells, and cultured T cells. EAC-rosettes (EAC-R), used to identify B lymphocytes with complement receptors, were prepared with normal PBL and cultured B cells. The majority of rosetting T lymphocytes had generally smooth surfaces while about 20% had an intermediate number of microvilli and 15% were more villous and indistinguishable from villous B cells. Studies of rosetting thymocytes and cultured T cells however indicated that the surface of some T cells alters on rosetting, becoming more villous and thus account for the higher numbers of villous T cells seen in E-rosettes. Point to point contact sites between SRBC and T lymphocytes were more frequent than broad zones of attachment. The majority of rosetting B lymphocytes had multiple microvilli, about 25% had a moderate number of microvilli and less than 10% had smooth surfaces similar to those of most T cells. Areas of contact between EAC and B lymphocytes were frequently broad zones of attachment. The study confirms that in many cases B and T lymphocytes can be distinguished by their surface architecture as seen under the SEM; however, about 20% of rosetting B and T cells have similar surfaces with intermediate numbers of surface microvilli and cannot be distinguished by SEM without parallel immunologic identification.

Animals↗
PubMed1974

Occurrence of surface IgM, IgD, and free light chains of human lymphocytes.

An analysis was made of the immunoglobulin surface markers of the cells of patients with chronic lymphatic leukemia (CLL) in view of previous evidence of their monoclonal B-cell character. The simultaneous presence of IgM and IgD on the surface of the majority of lymphocytes was demonstrated by both immunofluorescence and hemagglutination inhibition in most cases. However, cases were observed with surface IgM without IgD as well as cases with IgD without IgM. IgG and IgA were absent. Studies of the light chains indicated only a single class in a given case. In addition to bound light chains, free light chains were readily demonstrated in most cases through the use of antisera specific for "free chain" determinants. It thus appeared that there are three major types of surface Ig on CLL lymphocytes, IgM, IgD, and free light chains.

Animals↗
PubMed1974

Idiotypic specificity of surface immunoglobulin and the maturation of leukemic bone-marrow-derived lymphocytes.

Certain cases of chronic lymphocytic leukemia are associated with monoclonal immunoglobulins in the serum. In the present study it was possible to demonstrate that the surface immunoglobulin of the leukemic lymphocytes was idiotypically identical to the serum monoclonal immunoglobulin of the same individual. This was done through the use of fluorescent antibodies that were prepared against the isolated immunoglobulin M kappa serum protein from patient Ei. Such antibodies, after absorption, failed to react with the lymphocytes of other individuals. Capping experiments indicated that both the immunoglobulin M and the immunoglobulin D on the leukemic cells possessed the same idiotypic specificity.A population of plasma cells was also identified in the peripheral blood of patient Ei that showed strong intracellular staining with the idiotypic antiserum and was the apparent source of the specific serum immunoglobulin. The accumulated evidence indicates that the plasma cells were derived from the leukemic lymphocytes by a process of differentiation. Surface immunoglobulin D disappeared and surface immunoglobulin M decreased markedly in this process.

Aged↗
PubMedDate not supplied

Nature of cold-reactive antibodies to lymphocyte surface determinants in systemic lupus erythematosus.

Antilymphocyte antibodies in serum from patients with systemic lupus erythematosus (SLE), as detected by microcytotoxicity and indirect immunofluorescence, were predominantly cold reactive and of the IgM class. These IgM antibodies were most active at 4 degrees C. IgG antibodies were infrequent, and were only minimally lymphocytotoxic. Most sera were cytotoxic for autologous lymphocytes and were equally reactive with normal and SLE lymphocytes, as well as with B- and T-cell preparations. Separate T- and B-cell specificities, which appeared not to be related to HL-A determinants, were identified by differential absorption experiments. The functional significance of these antilymphocyte antibodies is discussed.

Animals↗
PubMedDate not supplied

Hereditary C2 deficiency: association with skin lesions resembling the discoid lesion of systemic lupus erythematosus.

Two patients with hereditary homozygous C2 deficiency are described. They showed many similar clinical features. Both had discoid-like skin rashes and serologic abnormalities consistent with SLE, but neither had evidence of involvement of any organ other than skin. Although biopsy of these lesions revealed expected changes by light microscopy, typical immunofluorescent findings were not present. The presence of the HL-A haplotype 10, W18 was seen in both families and was associated with the C2 deficiency gene. The 2 patients were mutually nonreactive in MLC tests and both were found to be homozygous for the LD7a type.

Adult↗
PubMedDate not supplied

Lupus glomerulonephritis revisited 2004: autoimmunity and end-organ damage.

Histopathology of the kidney and clinical presentation are critical factors in the diagnosis of immune-mediated glomerulonephritis (GN). The histological manifestations of glomerular injury are shared by multiple underlying mechanisms. Work from our laboratory and from other investigators shows that antinuclear, antihistone or anti-dsDNA antibodies are neither required nor sufficient for development of lupus GN. In addition, antibody to dsDNA can be generated by mechanisms other than loss of tolerance to chromatin. Genetic analyses demonstrate that although there is some interaction between autoantibody production and renal disease, the phenotypes are regulated by distinct genetic intervals. Furthermore, renal failure is not an essential outcome of the immune-complex deposition and proliferative lupus GN. These data are also supported by published studies from systemic lupus erythematosus (SLE) patients. The immune regulation of lupus GN is distinct from other organ-specific diseases and not influenced by CD25(+) or NK1.1(+) regulatory T cells. Thus, fatal GN may depend upon a kidney-reactive T-cell response that, in turn, may be regulated by gender and intrinsic end-organ factors. The data discussed in this review call for a re-evaluation of the current paradigms for pathogenesis of SLE. An interactive model separating autoimmunity from end-organ susceptibility for the pathogenesis of SLE is proposed.

Animals↗