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G C Koo

Publications and source records attributed to G C Koo.

At least 55 records · Page 3Linked to original sources
PubMed1984

Natural killer cells generated from bone marrow culture.

By using anti-Nk-1 antiserum, we detected a significant proportion of Nk-1+ cells in bone marrow (BM) with low lytic activity that can be slightly enhanced with interferon (IF). These BM Nk-1+ cells also bind to YAC-1 cells. Because Nk-1 antigen has been found to mark NK cells, BM appears to harbor immature precursors to natural killer (NK) cells. We therefore used concanavalin A (Con A)-conditioned medium to culture BM cells to induce differentiation of the putative NK precursors. After 3 to 4 days in culture, cytotoxic activity to YAC, that peaked at 6 to 7 days, was consistently generated, and the activity still could be detected after 10 to 14 days in culture. In contrast, experiments using spleen cultures, performed in a similar manner, showed peak activity after 4 to 5 days and the activity declined thereafter. The cytotoxic activity of cultured BM cells was also higher than that of cultured spleen cells. Cultures of BM cells from old mice have good cytotoxic activity. The cytotoxic cells generated were Nk-1+ and Qa-5+. Furthermore, these culture conditions did not maintain the proliferation of CFU-C cells.

Aging↗
PubMed1983

H-Y antigen in XO mice.

We examined the expression of H-Y antigen in 14 XO female mice using three monoclonal H-Y-specific antibodies. We found that spleen and liver cells from XO mice removed the reactivity of these antibodies at the same efficacy as XY cells. However radiobinding assays on cultured XO cells suggested a qualitative or quantitative difference between XO and XY cells. In cell-mediated cytolysis (CMC), H-Y-specific reactivity was observed when XO fibroblasts were used as targets, but no reactivity was observed when XO concanavalin A (Con A) blasts were used as targets. We concluded from these studies that XO mice do express H-Y antigen, detected both by serologic assays and cell-mediated assays.

Animals↗
PubMed1983

Fetal H-Y typing using human amniotic fluid.

The H-Y (male) antigen is phylogenetically conserved among vertebrate species, including the species man. Previous studies have indicated the presence of a "soluble" H-Y antigen in male serum and culture fluids of male cells. We examined over 50 samples of amniotic fluid from male and female fetuses to determine if H-Y typing could be correlated with the sex of the fetus. Samples of amniotic fluid were tested to inhibit the reactivity of monoclonal antibodies in a standard H-Y assay with protein A sheep red blood cells. We found that amniotic fluids from male fetuses inhibited 40% of the reactivity and that amniotic fluids from female fetuses inhibited 0.5% of reactivity. We could also correctly identify the sex of 90% of male fetuses and 100% of female fetuses. We have not yet identified the exact nature of the inhibiting antigen(s) in the amniotic fluids, but our results clearly indicate the feasibility of fetal H-Y typing.

Amniocentesis↗
PubMed1982

Ontogeny of Nk-1+ natural killer cells. I. Promotion of Nk-1+ cells in fetal, baby, and old mice.

Using anti-Nk-1.1 serum, the alloantiserum specific for murine natural killer (NK) cells, we followed the ontogenetic development of Nk-1+ cells in fetal thymus, liver, and spleen. A transient population of Nk-1+ cells in fetal thymus was observed on day 14 but not on day 16 of gestation. On day 16 of gestation, Nk-1+ cells were detected only in liver and spleen. The proportion of Nk-1+ cells in spleen remained high (20 to 30%) at birth and persisted until 2 to 3 wk old. The Nk-1+ cells in "baby" (1 to 2 wk old) spleen bound to YAC cells but failed to lyse them in 51Cr-release assay. Upon induction with interferon (IF), the proportion of Nk-1+ cells increased, but the lytic activity remained low, suggesting that the "baby" NK-1+ cells are immature in lytic function. In old mice (12 to 14 mo), Nk-1+ cells were also detectable, even though NK activities were lower compared with those of the young adult (6 to 8 wk old) mice. The Nk-1+ cells of old mice were readily induced by IF to exhibit activities, and the induced NK cells were Nk-1+. We have thus established Nk-1.1 antigen as an early hemopoietic differentiation antigen. Splenic Nk-1- cells could be induce by IF to become NK-1+ cells, which could be inactive or active in NK assays, dependent on the age of the mice.

Aging↗
PubMed1981

Application of monoclonal anti-HY antibody for human H-Y typing.

We have successfully produced monoclonal anti- H-Y antibody by fusing NS-1 myeloma cells with splenocytes from C57BL/6 females immunized with syngeneic male splenocytes. We have proved that the antibody is male specific and that it cross reacts with human H-Y. We have further tested 80 normal individuals for H-Y antigen and obtained significant differences between males and females. Therefore, the monoclonal anti- H-Y antibody is useful for clinical typing of human H-Y antigen.

Animals↗
PubMed1981

Serology of H-Y antigen.

Anti-H-Y antiserum is generally obtained from female inbred mice or rats that have been hyperimmunized with syngeneic male cells. The specificity of such antiserum is defined by its reactivity for male but not female cells. A number of conventional serological assays have been used to measure that reactivity. However, H-Y is a weak antigen, evidently represented sparingly on the surfaces of cells other than sperm, epidermal cells and brain cells ; thus the serological assays for H-Y are technically difficult. Yet H-Y serology has enabled significant progress toward the understanding of primary sex differentiation. A recent advance in H-Y serology is the establishment of monoclonal anti-H-Y antisera which promise to facilitate analysis and clarification of the H-Y system.

Animals↗
PubMed1981

Inhibition of H-Y cell-mediated cytolysis by monoclonal H-Y specific antibody.

Assays of H-Y specific, cell-mediated cytolysis (CMC) in vitro were carried out with B6 female effector cells and B6 male target cells. Monoclonal H-Y antibody was added to the lytic assay to test whether the antigenic determinant(s) involved in H-Y-specific CMC was distinct from the serologically detected H-Y antigen. Significant blocking was observed, suggesting that the H-Y antigen detectable serologically is similar to H-Y antigen recognized by cytotoxic T cells.

Animals↗
PubMed1981

Relation of gp70 to spontaneous cytolytic activity of mouse spleen cells.

In comparing spleen cells of inbred and congenic mice for spontaneous capacity to lyse cells of the BALB/c leukemia RLmale1 in vitro, we found that the activity of 129 spleen cells was more than double that of 129-Gix- spleen cells. The only known difference between these two strains is that 129-Gix- mice express no known demonstrable gp70 or p30, whereas 129 mice express both these MuLV-related components as mendelian traits not associated with the production of virions. We infer that MuLV-related components at the cell surface are concerned in effector-target interactions leading to cytolysis under the conditions described. Although the congenic strains B6 (Gix-) and B6-Gix+ differ likewise in expression of the type-variant Gix-gp70, both strains express a second type-variant of gp70. The lytic activity of spleen cells of these two strains for RLmale1 cells was equally high, suggesting that involvement in lytic effector-target interactions is common to gp70 molecules in general. When used as targets rather than as effectors 129 spleen cells were more sensitive to lysis than 129-Gix- spleen cells. Pre-exposure to gp70, purified from R-MuLV, rendered splenic effector cells less lytic. Pre-exposure to gp70 also rendered RLmale1 target cells less sensitive to lysis. One explanation of these findings is that both target cells and effector cells express gp70 and also receptors for gp70 and that this is the basis of mutual cellular recognition leading to lysis in the circumstances described.

AKR murine leukemia virus↗
PubMed1980

Abnormality of the X chromosome in human 46,XY female siblings with dysgenetic ovaries.

An abnormal extra band was found on the short arm of the X chromosome in a 46,XY female and in her 46,XY female fetal sibling. Despite presence of the intact Y chromosome, there was no evidence of testicular differentiation in either subject. Production of H-Y antigen was suppressed in both subjects. The data suggest that development of the mammalian testis requires a normal function of the X chromosome.

Female↗
PubMed1980

H-Y antigen in 46,XY gonadal dysgenesis.

Presence of H-Y antigen has been correlated with testicular differentiation, and absence of H-Y with failure of testicular differentiation, in a variety of mammalian species. To determine more precisely the relationship between expression of H-Y antigen and development of the testis, we studied the cells of phenotypic females with the 46,XY male karyotype. Blood leukocytes were typed H-Y+ in five XY females with gonadal dysgenesis, although in other studies blood leukocytes from XY females with gonadal dysgenesis were typed H-Y-. Thus mere presence of H-Y antigen is not sufficient to guarantee normal differentiation of the testis. In the present paper we review evidence for an additional factor in gonadal organogenesis, the H-Y antigen receptor. We infer that testicular development requires engagement of H-Y and its receptor. It follows that XY gonadal dysgenesis is the consequence of functional absence of the H-Y testis inducer as in the following conditions: failure of synthesis of H-Y or failure of specific binding of H-Y.

Adolescent↗
PubMed1980

Aberrant testicular differentiation in 46,XY gonadal dysgenesis: morphology, endocrinology, serology.

In an infant with gonadal dysgenesis and somatic anomalies, the internal and external genitalia were female but the gonads contained tubular structures suggesting male differentiation. The karyotype was 46,XY with no evidence of structural aberration or mosaicism. Hormonal metabolism and H-Y antigen expression were assayed in cultured gonadal cells. Although unable to synthesize testosterone, the cultured cells were able to convert it to dihydrotestosterone. H-Y antigen was present, perhaps at a level lower than that in cells from normal XY males. Our observations indicate that a modicum of testicular organogenesis may precede the involution that results in a streak gonad in some cases of gonadal dysgenesis.

Cells, Cultured↗
PubMed1980

H-Y antigen in X,i(Xq) gonadal dysgenesis: evidence of X-linked genes in testicular differentiation.

Three years ago, we detected H-Y antigen in the white blood cells of a phenotypic female with several of the stigmata of Turner's syndrome, and the mosaic karyotype: 45,X/46,X,i(Xq). We surmised at the time that the isochromosome, i(Xq), may have contained occult Y-Chromosome-derived material. We have now confirmed the presence of H-Y in this patient and we have obtained evidence for the presence of H-Y in four of five other similar patients, all of whom are notable for carrying at least a single cell line with the karyotype 46,Xi(Xq). Although we cannot categorically exclude the presence of Y-chromosomal genes in the cells of these patients, there is no cytogenetic evidence of structural rearrangement involving the Y in any of the cases. Expression of H-Y structural genes are X-situated, or alternatively that they are autosomal and X-regulated. It would follow that the H-Y+ cellular phenotype per se is not a valid marker for the Y-chromosome, and that H-Y genes that have been mapped to the pericentric region of the Y may be regulatory.

Adolescent↗
PubMed1980

Female phenotype and multiple abnormalities in sibs with a Y chromosome and partial X chromosome duplication: H--Y antigen and Xg blood group findings.

A mentally retarded female child with multiple congenital abnormalities had an abnormal X chromosome and a Y chromosome; the karyotype was interpreted as 46,dup(X)(p21 leads to pter)Y. Prenatal chromosome studies in a later pregnancy indicated the same chromosomal abnormality in the fetus. The fetus and proband had normal female genitalia and ovarian tissue. H--Y antigen was virtually absent in both sibs, a finding consistent with the view that testis-determining genes of the Y chromosome may be suppressed by regulatory elements of the X. The abnormal X chromosome was present in the mother, the maternal grandmother, and a female sib: all were phenotypically normal and showed the karyotype 46,Xdup(X)(p21 leads to pter) with non-random inactivation of the abnormal X. Anomalous segregation of the Xga allele suggests that the Xg locus was involved in the inactivation process or that crossing-over at meiosis occurred.

Abnormalities, Multiple↗
PubMed1980

Antigenic profile of murine natural killer cells.

We have determined the antigenic profile of natural killer (NK) cells from C57BL/6 mice that have lytic activity to RLmale1 tumor cells, in a 5-hr 51Cr release assay. To perform the antigenic typing more effectively, we enriched the NK populations by using discontinous BSA density gradient and established a correlation between NK activity and NK-1 antigen in each layer. As NK activity and Nk-1 antigen are both criteria for measuring NK cells, we determined the antigenic profile of NK cells by monitoring both the change in NK activity and NK-1 cells, after elimination of cells with various antisera to lymphocytic alloantigens. We have found that all NK cells expressed Nk-1, Qa-4, and Qa-5 antigens; about 50% of NK cells expressed Thy-1 and Qa-2 antigens, and 25% of NK cells also expressed Lyt-1 antigen. NK cells did not express significant amounts of Qa-1, Qa-3, Lyt-2, and Lyb-2 antigens. Therefore, spontaneous NK cells are heterogeneous with regard to their surface antigens, some of which are T cell antigens. However, the present antigenic profile does not allow us to classify NK cells in the conventional T cells lineage.

Animals↗
PubMed1979

Inhibition of H-Y cell-mediated cytolysis by H-2Db antiserum.

Assays of H-Y-specific cell-mediated cytolysis (CMC) in vitro were carried out with B6 female effector cells and B6 male target cells. This lytic system depends on compatibility for H-2Db but not for H-2Kb. Antibody to H-2Db but not to H-2Kb blocked the CMC assay. However, maximal blocking required exposure to the target cells to H-2Db antibody for up to 2 h. This interval is far longer than would be required for blocking of a pre-existing H-Y:H-2Db complex, and seems more consonant with a membrane reorganization bringing H-Y and H-2Db together, as proposed from mapping studies. The question whether the postulated configurational change affecting H-Y and H-2Db is a necessary feature of CMC awaits further study.

Animals↗
PubMed1979

H-Y antigen mosaicism in the gonad of a 46,XX true hermaphrodite.

To clarify the mechanism for the coexistence of ovarian and testicular tissue in the 46,XX true hermaphrodite, we studied a 20-year-old phenotypic male with gynecomastia and elevated serum concentrations of estradiol in whom an ovotestis was discovered upon scrotal exploration. Y chromosomal material could not be detected by fluorescent Y-body analysis or Giemsa-banding technics in cells cultured from peripheral blood, breast or forearm skin or the ovarian or testicular portions of the ovotestis. However, serologic testing, using the sperm cytotoxicity assay, revealed that cells cultured from the testicular portion of the ovotestis were H-Y antigen positive whereas cells cultured from the ovarian portion were H-Y antigen negative. These observations indicate that the ovotestis arises from an H-Y+/H-Y- mosaic primordium.

Adult↗
PubMed1979

Sexual and somatic determinants of the human Y chromosome: studies in a 46,XYp- phenotypic female.

A case of a 46,XYp- phenotypic female provided an opportunity to evaluate both sexual and somatic determinants for the Y chromosome. The patient had multiple stigmata of Turner syndrome, but normal stature. Laparotomy revealed a normal uterus and tubes, with 1.5 cm undifferentiated gonads. Serological tests for H-Y antigen (ostensibly the product of Y-chromosomal testis-determining genes) indicated absence of the H-Y+ phenotype normally associated with the intact Y chromosome. We conclude that genes exist on the short arm of the human Y chromosome which both suppress some of the somatic stigmata of Turner syndrome and determine normal expression of H-Y antigen and testicular differentiation of the primitive gonad. Our data are consistent with the view that H-Y genes comprise a family of testis-determinants, and that loss of a critical moiety is inconsistent with normal development of the male gonad.

Body Height↗