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At least 19 recordsLinked to original sources

PubMed1991

Characterization of an established mouse-human heterohybridoma and its application for production of (mouse-human)-human triple hybridoma secreting human immunoglobulin.

We report the construction of a mouse-human (M-H) heterohybridoma by fusion of the murine myeloma cell line NS-1 and human spleen cells from a 17 week old fetus. The nonsecreting, cloned hybridoma cell line II was resistant to 8-azaguanine (8-AG) and sensitive to hypoxanthine, aminopterin and thymidine (HAT) medium. It grew rapidly in 8-AG containing medium (doubling time 20 hrs.), but did not grow in HAT medium or in non-serum medium. It had a high fusion frequency with human lymphocytes from regional lymph nodes. Five human chromosomes were retained stably for over 6 months by this cell line II. Nine (mouse-human)-human ((M-H)-H) triple hybridomas secreting human IgG 1 or IgM were established by the fusion of this parental cell line II and human lymphocytes from regional lymph nodes. Immunoglobulin secretion was stable and has been maintained for over 8-10 months without recloning in these hybridomas. Secretion of immunoglobulin varies from 2.1-3.0 micrograms/10(6) cells/day, and these hybridomas contain from 3 to 16 human chromosomes, including No. 14. So, this M-H heterohybridoma II is an excellent useful parental cell line for the production of hybridomas secreting human immunoglobulin.

Animals↗

PubMed1990

Autoantibodies to crude human leucocyte interferon (IFN), native human IFN, recombinant human IFN-alpha 2b and human IFN-gamma in healthy blood donors.

Recently, naturally occurring antibodies to IFN-alpha were discovered in a few systemic lupus erythematosus (SLE) and cancer patients; however, in most patients monitored for anti-IFN antibodies before treatment, no antibodies were found. In an attempt to explain the 'IFN-blocking effect' that we observed in all serum samples we investigated 200 sera from healthy blood donors. We isolated the globulin fraction, and used rabbit anti-human IgG and IgM columns, protein A columns and T-gel affinity chromatography to isolate human IgG and IgM. All sample fractions were tested in a biological IFN neutralization assay by means of a sensitive MTT-assay. We found that normal human serum contained autoantibodies to crude human leucocyte IFN, native human fibroblast IFN, recombinant human leucocyte IFN-alpha 2b and recombinant human IFN-gamma, and that these naturally occurring antibodies were biologically active immunoglobulins of IgG and IgM type. These anti-IFN antibodies were also present in purified human normal immunoglobulin pools. We conclude that all humans have naturally occurring anti-interferon antibodies in their serum, and it is a tempting theory that human cytokines and lymphokines are, at least partly, regulated by immunoglobulins.

Adolescent↗

PubMed1990

Pokeweed mitogen-stimulated human lymphocytes fused to LICR-2 (HMY2) generate human-human hybridomas producing monoclonal IgG antibodies reactive to human breast carcinoma and malignant melanoma.

Human-human hybridomas were generated using pokeweed mitogen-stimulated lymphocytes from the regional lymph nodes of cancer patients by fusion to the LICR-2 human myeloma cell line. A total of 35 fusions, using the regional lymph node lymphocytes of cancer patients, resulted in hybrid growth in 23% of wells plated with 21 IgG ELISA positive clones, 6 of which have maintained stable human monoclonal antibody production. Mononuclear cells were separated on Ficoll-Paque and grown for 3-4 days in 1% pokeweed mitogen and fused to the LICR-2 human myeloma cell line. Human-human hybridoma producing membrane reactive IgG antibodies have been isolated and react to the following cancers: breast; melanoma. Twenty-seven fusions from 8 breast carcinoma patients resulted in 13 ELISA positive IgGs, 3 of which were stable after cloning. A total of 5,071 wells were plated after polyethylene glycol fusion with resultant hybrid growth in 1210 wells (24% hybrid growth) after hypoxanthine-aminopterin-thymidine selection. In 8 fusions using regional lymph node lymphocytes of other types of cancer, including 6 fusions using lymphocytes from malignant melanoma patients, there were 1,580 wells plated with positive growth in 20% of the wells (311 wells). Of these, 8 clones were ELISA positive and 3 stable clones all producing IgG anti-melanoma antibody were isolated. The overall hybrid frequency was 43 x 10(-7) fused lymphocytes (39 x 10(-7) non-breast and 45 x 10(-7) breast). A total of 21 IgG-producing clones were identified to crude membranes of allogeneic tumor cell lines and stable antibody production was achieved for 6 (29% stable clones).(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Monoclonal↗

PubMed1986

Effects of recombinant human tumor necrosis factor alpha, recombinant human gamma-interferon, and prostaglandin E on colony formation of human hematopoietic progenitor cells stimulated by natural human pluripotent colony-stimulating factor, pluripoietin alpha, and recombinant erythropoietin in serum-free cultures.

The influences of pure human pluripotent colony-stimulating factor, highly purified pluripoietin alpha, pure recombinant human tumor necrosis factor alpha, pure recombinant human gamma-interferon, and natural prostaglandin E1 (PGE1) were evaluated on colony formation of multipotential and erythroid progenitor cells in the presence of recombinant erythropoietin and hemin and on colony formation of granulocyte-macrophage progenitors in normal human marrow cultured in the presence or absence of serum. Serum was replaced by bovine serum albumin, iron-saturated transferrin, cholesterol, and calcium chloride. Increasing concentrations of pluripotent colony-stimulating factor and pluripoietin alpha stimulated increasing numbers of colonies from nonadherent low-density T-lymphocyte-depleted cells in the absence and presence of serum. Growth was usually greater in the presence of serum and on a unit basis pluripoietin alpha was more active than pluripotent colony-stimulating factor. Recombinant human tumor necrosis factor alpha and recombinant human gamma-interferon suppressed colony formation colony forming unit-granulocyte-macrophage, burst forming unit-erythroid, and colony forming unit-granulocyte-erythroid-macrophage-megakaryocyte; PGE1 suppressed colony formation by colony-forming unit-granulocyte-macrophage, stimulated colony formation by burst forming unit-erythroid, and had no effects on colony formation by colony forming unit-granulocyte-erythroid-macrophage-megakaryocyte in both serum-containing and serum-free medium. The PGE1 enhancing effects on erythroid colony formation required T-lymphocytes. Thus, results are similar using serum-containing and serum-free cultures of human bone marrow cells and serum-free defined culture medium can be used to study the mechanism of action of purified natural and recombinant growth and suppressor molecules in vitro.

Bone Marrow Cells↗

PubMed1992

Existence of PAF receptors in human platelets and human lung tissue but not in the human myocardium.

The aim of this study was to investigate whether platelet-activating factor (PAF), PAF receptors, and PAF receptor-mediated effects in the human myocardium play a role in cardiac depression during anaphylaxis or septic shock. The effects of PAF, the biologically inactive derivative lyso-PAF, and the specific PAF antagonist WEB 2086 were studied in human myocardial tissue, in human coronary arteries, in human platelets, and in human lung tissue. PAF (C16-PAF, C18-PAF; 0.000001 to 1 mumol/L) had no effect on isometric force of contraction of electrically driven right atrial trabeculae (patients undergoing aortocoronary bypass surgery) and left ventricular papillary muscle strips (mitral valve replacement). PAF (0.2 mumol/L) did not influence the concentration-response curve of either the beta-adrenoceptor agonist isoprenaline (ISO, 0.0001 to 1 mumol/L) or the m-cholinoceptor agonist carbachol (CARB, 0.0001 to 10 mumol/L). The effectiveness (ISO +4.7 +/- 0.7 mN, PAF + ISO + 4.3 +/- 0.44 mN, CARB -2.7 +/- 1.06 mN; PAF + CARB -2.6 +/- 0.52 mN) and the potency--as indicated by the EC50 values--of both isoprenaline and carbachol were identical with and without pretreatment with PAF (0.2 mumol/L). PAF at concentrations of 0.000001 to 10 mumol/L exerted no effect on force of contraction either precontracted (prostaglandin F2 alpha, 0.3 mumol/L) or unprecontracted in human coronary artery rings. Histamine (0.01 to 100 mumol/L) and noradrenaline (0.001 to 30 mumol/L) initiated concentration-dependent contraction in human coronary artery rings (EC50: histamine, 1.86 mumol/L; noradrenaline, 0.69 mumol/L). At lower concentrations (PAF, 0.01 mumol/L) PAF produced complete aggregation of human platelets. In human platelet membranes and lung membranes, 3H-WEB 2086 exhibited saturable high-affinity binding (KD 14.4 nmol/L and 14.3 nmol/L). The maximal binding capacity was 292 fmol/mg protein and 268 fmol/mg protein, respectively. In displacement experiments PAF (0.01 to 10000 nmol/L) and WEB 2086 (0.01 to 10000 nmol/L), but not lyso-PAF, completely displaced 3H-WEB 2086 from its binding sites on human and lung membranes. In contrast, neither in left ventricular membranes nor in right atrial membranes was specific binding of 3H-WEB 2086 observed. These results suggest that there are neither specific PAF receptors nor direct PAF-mediated actions in human myocardial tissue or human coronary artery rings. The effects of PAF on myocardial function may be due to the activation of mediators (e.g., histamine).

Azepines↗

PubMed1989

Defective repair of UV-damaged DNA in human tumor and SV40-transformed human cells but not in adenovirus-transformed human cells.

The DNA repair capacities of five human tumor cell lines, one SV40-transformed human cell line and one adenovirus-transformed human cell line were compared with that of normal human fibroblasts using a sensitive host cell reactivation (HCR) technique. Unirradiated and UV-irradiated suspensions of adenovirus type 2 (Ad 2) were assayed for their ability to form viral structural antigens (Vag) in the various cell types using immunofluorescent staining. The survival of Vag formation for UV-irradiated Ad 2 was significantly reduced in all the human tumor cell lines and the SV40-transformed human line compared to the normal human fibroblasts, but was apparently normal in the adenovirus-transformed human cells. D0 values for the UV survival of Ad 2 Vag synthesis in the tumor and virally transformed lines expressed as a percentage of that obtained on normal fibroblast strains were used as a measure of DNA repair capacity. Percent HCR values ranged from 26 to 53% in the tumor cells. These results indicate a deficiency in the repair of UV-induced DNA damage associated with human tumorigenesis and the transformation of human cells by SV40 but not the transformation of human cells by adenovirus.

Adenoviruses, Human↗

PubMed1991

Human interleukin-9: genomic sequence, chromosomal location, and sequences essential for its expression in human T-cell leukemia virus (HTLV)-I-transformed human T cells.

We have isolated the genomic sequence of human interleukin-9 (IL-9) based on its sequence homology with a human IL-9 cDNA isolated from human T-cell leukemia virus (HTLV)-I-transformed T cells by expression cloning. The entire genomic sequence has been determined and the gene consists of five exons and four introns. The human IL-9 gene is mapped to the long arm of human chromosome 5 at band 5q31-32, a region found to be deleted in a number of patients with acquired 5q- abnormalities and hematologic disorders. Several blocks of transcriptional control sequences have been identified at the 5'-flanking region of the human IL-9 gene that may play an important role in the control of IL-9 gene expression. The 5'-regulatory region of the human IL-9 gene also contains sequences identified in the 5'-flanking regions of other cytokine genes mapped to the long arm of human chromosome 5, including IL-3, IL-4, IL-5, and granulocyte-macrophage colony-stimulating factor and other T-cell growth factor genes including IL-2 and IL-6. The IL-9 gene is constitutively expressed in the HTLV-I-transformed human T cells and the expression of IL-9 in these cells can be further induced by 12-O-tetradecanoyl phorbol 13-acetate. Transient transfection analysis using the plasmid containing the 5'-flanking region of IL-9 gene upstream from the firefly luciferase ciferase report gene indicated that the 0.9-kb Smal-Sacl fragment of the IL-9 gene contains sequences required for the constitutive and activated expression of IL-9 gene in HTLV-I-transformed cells. These results will now allow us to study the regulatory mechanism of IL-9 gene expression in normal and leukemic human T cells.

Amino Acid Sequence↗

PubMed1991

Characterization of the human liver vasopressin receptor. Profound differences between human and rat vasopressin-receptor-mediated responses suggest only a minor role for vasopressin in regulating human hepatic function.

The [Arg8]vasopressin (AVP) receptor expressed by human hepatocytes was characterized, and compared with the rat hepatic V1a vasopressin receptor subtype. In addition to determining the pharmacological profile of the human receptor, the cellular responses to AVP were measured in human and rat hepatocytes by assaying glycogen phosphorylase alpha activity and DNA synthesis. Marked differences were observed between human and rat hepatocytes regarding vasopressin receptors and the intracellular consequences of stimulation by AVP. Data presented in this paper demonstrate the following, (i) Vasopressin V1a receptors are present in low abundance on human hepatocytes. (ii) Species differences exist between human and rat V1a receptors with respect to the affinity of some selective antagonists. (iii) AVP-stimulated glycogen phosphorylase a activation in human hepatocytes was approx. 5% of that observed in rat cells. (iv) In contrast with rat hepatocytes, DNA synthesis in human cells in culture was not stimulated by AVP. It is concluded that vasopressin plays only a minor role in the regulation of human hepatic function. Furthermore, conclusions drawn from observations made with AVP and its analogues on rat hepatic function cannot be directly extrapolated to the human situation.

Animals↗

PubMed1987

Human pituitary and placental hormones control human insulin-like growth factor II secretion in human granulosa cells.

Human granulosa cells cultured with calf serum actively proliferated for 18-20 generation and secreted progesterone into the medium; progesterone levels appeared to decline with increase in generation number. Cells cultured under serum-free conditions secreted significant amounts of progesterone and insulin-like growth factor II (IGF-II). The progesterone secretion was enhanced by the addition of human follitropin, lutropin, and chorionic gonadotropin but not by growth hormone. These cells, when challenged to varying concentrations of human growth hormone, human chorionic somatomammotropin, human prolactin, chorionic gonadotropin, follitropin, and lutropin, secreted IGF-II into the medium as measured by specific IGF-II RIA. Among these human hormones, chorionic gonadotropin, follitropin, and lutropin were most effective in inducing IGF-II secretion from these cells. When synthetic lutropin-releasing hormone and alpha-inhibin-92 were tested, only lutropin-releasing hormone was effective in releasing IGF-II. The results described suggest that cultured human granulosa cells can proliferate and actively secrete progesterone and IGF-II into the medium. IGF-II production in human granulosa cells was influenced by a multi-hormonal complex including human growth hormone, human chorionic somatomammotropin, and prolactin.

Cells, Cultured↗

PubMed1992

Recombinant human growth hormone promotes human lymphocyte engraftment in immunodeficient mice and results in an increased incidence of human Epstein Barr virus-induced B-cell lymphoma.

Recombinant human growth hormone (rhGH) previously has been demonstrated to promote human or mouse T-cell engraftment in immunodeficient mice. We then wanted to examine long-term effects of rhGH on human cell engraftment in these mice. Mice with severe combined immune deficiency (SCID) were given human peripheral blood lymphocytes or human bone marrow cells and daily injections of rhGH (20 micrograms ip every other day). Upon later assessment for engraftment by flow cytometric analysis, it was determined that rhGH strongly promoted human T-cell engraftment in the thymus and spleens of these mice. However, there was considerable variability in both the incidence and extent of engraftment which appears to be due to donor-to-donor variation. Additionally, rhGH promoted B lymphomagenesis in these mice since long-term treatment of these xenogeneic chimeras with rhGH resulted in the increased incidence of human Epstein-Barr virus (EBV)-infected B-cell lymphoma. Thus, while rhGH can be used to optimize human T-cell engraftment in SCID mice, it also increases the likelihood of B-cell lymphoma generation when the donor is EBV infected. The results suggest that the activation of human T cells by rhGH results in an increased ability of these cells to traffic to the peripheral lymphoid organs of the SCID mice and results in a lymphoid microenvironment conducive to the outgrowth of EBV-transformed B lymphocytes.

Animals↗

PubMedDate not supplied

The recombinant human interferon-gamma receptor is fully functional in a human x murine hybrid containing human chromosome 21.

It has previously been shown that stimulation of class I MHC antigen expression by human interferon gamma (Hu-IFN gamma) depends on the presence of both human chromosomes 6 and 21. Even although the presence of human chromosome 6 results in normal expression of the IFN gamma receptor on the cell surface, chromosome 21 is required for this biological response. Here, we transfected the cDNA encoding the Hu-IFN gamma receptor into a mouse cell line, L(tk-), and into a mouse x human hybrid, GM08, containing the human chromosome 21 as the only human genetic material. Two clones, L-gamma R.8 and GM08-gamma R.9, were tested for different biological responses to Hu-IFN gamma. Only the hybrid containing the human chromosome 21 (GM08-gamma R.9) exhibited a biological response when assayed for the stimulation of murine class I MHC antigen expression by Hu-IFN gamma. Moreover, transcriptional induction of 2'-5'-oligoadenylate synthetase and 1-8 genes, as well as antiviral protection, were observed only in the GM08-gamma R.9 transfectants. These results show that human chromosome 21 encodes a factor which mediates different biological activities of Hu-IFN gamma.

Blotting, Northern↗

PubMed1976

Do highly oncogenic group A human adenoviruses cause human cancer? Analysis of human tumors for adenovirus 12 transforming DNA sequences.

Adenovirus 12 (Ad12) (Huie) (highly oncogenic group A) readily induces tumors in newborn rodents. Since Ad12 is isolated from human fecal samples, we investigated whether it plays a role in the etiology of human gastrointestinal cancer. If Ad12 is a causal agent of human cancer, then human tumors should contain Ad12 transforming genes, as indicated by studies of cells transformed in vitro and in vivo by oncogenic viruses. Ad12 DNA and the Ad12 transforming restriction fragment (EcoRI-C fragment, left 16% of the viral genome) were labeled in vitro to 10(7) to 4 X 10(8) cpm/mug by the nick translation reaction of DNA polymerase of Escherichia coli. The fidelity and sensitivity of these probes were established by (i) analysis of DNA from Ad12-transformed cells and from hamsters with tumors induced by Ad12, (ii) reconstruction experiments with added Ad12 DNA and EcoRI restriction fragments, and (iii) comparison of annealing characteristics with Ad12 probes labeled in vivo. With Ad12 [3H]DNA as probe, no viral DNA sequences were detected in 18 normal gastrointestinal tissues and 34 gastrointestinal tumors, including cancers of the colon, rectum, small intestine, and stomach, under conditions that would detect 0.1 copy of the Ad12 genome per tumor cell. Similar analyses of Ad12-transformed hamster cells and Ad12 primary hamster tumors indicated 6-18 copies per cell of over 90% of the viral genome. With the Ad12 EcoRI-C transforming fragment as probe, no hybridization was detected with 32 human gastrointestinal tumors and five normal tissues; this result excludes 1-2% of the Ad12 genome per tumor cell. Our date are strong evidence that Ad12 is not a major cause of human gastrointestinal cancer. The Ad12 transforming EcoRI-C fragment hybridized (50-68% efficiency) with other Ad12 isolates and with Ad18 and 31 (members of oncogenic group A), but not at all with 28 other human Ad serotypes (manuscript in preparation). Thus other group A members probably are also not involved in human gastrointestinal cancer. No viral DNA sequences were detected in 12 normal lungs and 22 lung tumors, suggesting that respiratory cancer does not involve an Ad12 etiology.

Adenoviruses, Human↗

PubMed1987

Production and characterization of human-human and human-mouse hybridomas secreting Rh(D)-specific monoclonal antibodies.

Human monoclonal antibodies specific for the Rh(D) antigen were produced by cell lines generated by the fusion of pooled Epstein-Barr virus (EBV)-transformed B-cell lines secreting Rh(D) antibodies with the murine myeloma cell line NS.1 or with the human lymphoblastoid cell line HOA.1. The selection of hybrids was achieved in RPMI 1640 medium containing HAT and ouabain. Higher fusion efficiency was obtained with the NS.1 cell line; however, the hybrids with HOA.1 exhibited a greater clonal stability. The products of four clones (three human-human and one human-mouse) that consistently secreted antibodies for over 11 months were tested for specificity with a panel of red cells of various Rh phenotypes. The supernatants of all four clones showed anti-Rh(D) specificity but failed to react with the red cell Du phenotypes categorized as DV(Dw+) and DVI. Two of the three human-human clones secreted IgM(lambda) and the third IgG(kappa). The human-mouse clone produced IgG(kappa) antibody.

Animals↗

PubMed1978

Effects of insulin, human placental lactogen and human growth hormone of DNA synthesis in organ cultures of benign human breast tumours.

Nineteen benign human breast tumours, from 19 premenopausal patients, were processed into slices and each tumour was individually cultured for 2 days in Medium 199. The effects of bovine insulin (5.0 microgram/ml) human placental lactogen (10.0 microgram/ml) and human growth hormone (10.0 microgram/ml) on 3H-thymidine incorporation into DNA were determined on the cultured tumour slices. Insulin and human placental lactogen significantly (P less than 0.01) increased the mean incorporation of [3H]TdR into DNA, whereas human growth hormone was ineffective. These results provide evidence that insulin and human placental lactogen, but not human growth hormone, may be important factors in the aetiology of benign human breast tumours.

Breast Neoplasms↗

PubMed1990

Alloimmunization with cultured human stomach cancer cell lines and the establishment of human-human hybridomas producing monoclonal antibodies.

Alloimmunization with the cultured human stomach cancer cell lines MKN-45 and MKN-28 was conducted and human-human hybridomas were established. Living MKN-45 cells (10(7) cells per injection) were injected monthly 34 times into one of the authors (K.K.) over 2 years and living MKN-28 cells (10(7) cells per injection) were co-injected 14 times after the 20th injection of MKN-45 alone. Cultured stomach cancer cells injected subcutaneously into K.K.'s forearm were rejected completely, although they grew transiently at the injection site. All the injections were made voluntarily at the direction of K.K. himself. Two human-human hybridomas producing monoclonal antibodies reactive with MKN-45 and MKN-28 cells, respectively, were separated from a hybridoma of human B-lymphoblastoid cell line named HO 323/WIL2-NS and lymphocytes in K.K.'s peripheral blood. One cell line of the hybridoma FMK-H3 produced IgM-type monoclonal antibody, and the other line, EMK-F7, produced IgG-type antibody. These two human-human monoclonal antibodies were highly reactive with MKN-45 and MKN-28 cells, weakly reactive with MKN-74 stomach cancer cell line, and not reactive with the other stomach cancer cell lines tested (MKN-1, MKN-7, TMK-1, NUGU-2, NUGC-3, NUGC-4 and KATO-III).

Adenocarcinoma↗

PubMed1991

The biological activity of bovine and human thyrotropin is differently affected by trypsin treatment of human thyroid cells: thyroid-stimulating antibody is related to human thyrotropin.

Pretreatment of cultured human thyroid cells with trypsin decreased the cAMP response to bovine TSH (bTSH) (by 50-60%). In striking contrast, in trypsin treated cells the cAMP stimulation by both human TSH (hTSH) and thyroid-stimulating antibodies (TSab) was unimpaired, indicating a similar behavior for these two stimulators. The effect of trypsin on inhibiting cAMP stimulation by bTSH was: 1) dose dependent; 2) present at a trypsin concentration as low as 3.3 mg/L; 3) fully reversible within 24 h after removal of the enzyme. In accordance with the altered biological activity in human thyroid cells exposed to trypsin the binding of labeled bTSH was reduced (about 40%). On the contrary, in the same cells, the binding of labeled human TSH was enhanced (about 3-fold). The cAMP response to cholera toxin and forskolin was unaffected in trypsin treated cells, indicating that the tryptic treatment did not alter any other component of the adenylate cyclase complex. The medium obtained from trypsin-treated human thyroid cells was able to neutralize the biological activity of bTSH but not that of hTSH or TSab. Our study demonstrates that in human thyroid cells: 1) trypsin impaires bovine, but not human TSH or TSab biological activity; 2) bovine and human TSH may bind to different components of the TSH receptor.

Animals↗

PubMed1991

Human lung-derived mature mast cells cultured alone or with mouse 3T3 fibroblasts maintain an ultrastructural phenotype different from that of human mast cells that develop from human cord blood cells cultured with 3T3 fibroblasts.

Culture systems designed to maintain or develop human mast cells have proved difficult, yet these systems would provide valuable resources for future investigations of human mast cell biology. Cocultures of either isolated mature human lung mast cells (Levi-Schaffer et al., J Immunol 1987, 139:494-500) or human cord blood mononuclear cells (Furitsu, Proc Natl Acad Sci USA 1989, 86:10039-10043) with 3T3 embryonic mouse skin fibroblasts have implicated fibroblasts as an important factor in the successful maintenance and development of human mast cells in vitro. The authors cultured isolated, mature human lung mast cells either with or without 3T3 cells for 1 month and examined their ultrastructural phenotype. Mast cell viability in each circumstance was equivalent, but mast cell yield was improved in the presence of 3T3 cells. The ultrastructural phenotype was identical in both culture systems. Mast cells were shown to maintain the phenotype of their in vivo lung counterparts (ie, scroll granules predominanted, and numerous lipid bodies were present). This ultrastructural phenotype differs from that of mast cells that develop in cocultures of human cord blood cells and 3T3 cells, where developing mast cells with crystalline granules and few lipid bodies prevail, a phenotype much like that of human skin mast cells in vivo (Furitsu, Proc Natl Acad Sci USA 1989, 86:10039-10043).

3T3 Cells↗

PubMed1978

Lung uptake to technetium-99m microaggregated human albumin in the rat after treatment with microaggregated human albumin or macroaggregated human albumin.

Marked accumulation in lung and liver of intravenously--injected 99mTc-microaggregated human serum albumin (liver imaging agent) was observed in rats pretreated with the subcutaneous injection of microaggregated or macroaggregated human serum albumin, whereas accumulation of 99mTc-microaggregated human serum albumin was observed only in the liver of rats pretreated with plain human serum albumin or in non-treated control rats. The activity of the intravenously-administered 99mTc-sulfur colloid was concentrated in the liver and spleen only and not in the lung, of rats previously treated with human serum albumin, microaggregated human serum albumin, or macroaggregated human serum albumin. These observations suggest that the specific accumulation of microaggregated human serum albumin in the lung of rats pretreated with aggregated albumin is due to rapid in vivo clumping of injected particles, possibly due to antigen-antibody reaction.

Animals↗