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At least 73 records · Page 4Linked to original sources
PubMed1995

Acutely infected Langerhans cells are more efficient than T cells in disseminating HIV type 1 to activated T cells following a short cell-cell contact.

Most human immunodeficiency virus type 1 (HIV-1) infections involve sexual contact and virus passage across mucosal surfaces. While Langerhans cells (LCs) and dendritic cells (DCs) have been implicated in mucosal infection, their role is undefined. Here we demonstrate that acutely HIV-1-infected LCs and DCs effectively transmit virus to uninfected, activated T cells. Cocultivation of these cells results in massive virus production that requires a short cell-cell contact; as little as 30 min contact time is sufficient for HIV-1-pulsed DCs to infect their target T cells. Furthermore, surface-bound virus inactivation by trypsin does not significantly decrease the efficiency of virus transmission by LC/DCs, suggesting rapid internalization of virus. This effective virus transfer by infected LCs and blood-derived DCs requires prior activation of T cells. Surprisingly, cocultivation of acutely infected T cells with uninfected, activated target T cells results only in low virus production, even with T cell-tropic virus. We conclude that LCs and DCs are not only important targets of HIV-1 infection, but may also play a key role in the early dissemination of virus to T cells they encounter in skin or lymphoid tissue.

Cells, Cultured↗
PubMed1998

Mutual education between hematopoietic cells and bone marrow stromal cells through direct cell-to-cell contact: factors that determine the growth of bone marrow stroma-dependent leukemic (HB-1) cells.

A stroma-dependent cell line (HB-1) was established from myelogenous leukemic cells of CBA/N mouse. Characterization of the cells showed that HB-1 proliferated on hematopoietic supportive stromal cells (MS-10), but did not survive or proliferate on hematopoietic nonsupportive cells (MS-K). Direct contact between HB-1 and MS-10 appears to be necessary for HB-1 to proliferate on MS-10. We found that interleukin-1alpha (IL-1alpha) produced by MS-10 plays a major role in the survival and proliferation of HB-1. IL-11 did not support the proliferation of HB-1 cells by itself, but enhanced the proliferation of HB-1 cells in the presence of IL-1alpha. The expression of IL-1alpha and IL-11 was induced in MS-10 by the direct contact with HB-1 cells, and the expression of IL-1 receptor type I (IL-1RI) and interleukin-11 receptor (IL-11R) was induced in HB-1 cells by the attachment of the cells to MS-10. These findings show the existence of two-way interactions between HB-1 and MS-10.

Acute Disease↗
PubMed1987

Distribution of microtubules and microfilaments in exocrine (ventral prostatic epithelial cells and pancreatic exocrine cells) and endocrine cells (cells of the adenohypophysis and islets of Langerhans). The relationship between cytoskeletons and epithelial-cell polarity.

We investigated the distribution of microtubules and microfilaments in some exocrine and endocrine cells in rats. Microtubules were stained by applying an immunofluorescent technique using antibodies against beta-tubulin, while microfilaments were stained with rhodamine-phalloidin, which binds selectively to polymerized actin filaments. In the cytoplasm of some exocrine cells (pancreatic acinar cells and ventral prostatic epithelial cells), the microtubules were distributed longitudinally from the apical region to the basal region, but no microtubules were found in the nuclear region. In exocrine cells, most of the microfilaments were localized beneath the apical plasma membrane. In some endocrine cells (those of the adenohypophysis and the islets of Langerhans), the microtubules exhibited a radial or reticular distribution in the cytoplasm, and intense fluorescence was observed in the perinuclear region. The immunofluorescence produced by the antibodies against beta-tubulin was more intense in endocrine cells than in exocrine cells. The microfilaments observed in the endocrine cells studied were homogenously distributed beneath the plasma membrane. Dot-like rhodamine-phalloidin staining was often observed in the cytoplasm of both the exocrine and endocrine cells. The present study clearly demonstrated marked differences in the distribution of cytoskeletal elements in exocrine and endocrine cells, and these may reflect differences in the secretory direction of such cells as well as in epithelial-cell polarity.

Actin Cytoskeleton↗
PubMed1988

Cell to cell adhesion systems in Xenopus laevis, the South African clawed toad. II: Monoclonal antibody against a novel Ca2+-dependent cell-cell adhesion glycoprotein on amphibian cells.

We isolated a mouse monoclonal antibody that disrupts Ca2+-dependent cell-cell adhesion of amphibian (Xenopus laevis) cells. When added to culture medium, the monoclonal antibody completely disrupted cell-cell adhesion of amphibian cells in monolayer culture and specifically inhibited Ca2+-dependent cell-cell adhesion of dissociated cells in reaggregation experiments. The monoclonal antibody recognized a 140 kDa cell surface glycoprotein antigenically different from the previously reported Ca2+-dependent cell-cell adhesion molecules (cadherins).

Animals↗
PubMed2004

FcepsilonRI engagement of Langerhans cell-like dendritic cells and inflammatory dendritic epidermal cell-like dendritic cells induces chemotactic signals and different T-cell phenotypes in vitro.

BACKGROUND: Atopic dermatitis (AD) is a biphasic inflammatory skin disease characterized by an initial phase predominated by T(H)2 cytokines, which switches into a second T(H)1-dominated chronic phase. Thus far, the small number of FcepsilonRI-bearing Langerhans cells (LCs) and inflammatory dendritic epidermal cells (IDECs) in the epidermis of patients with AD has hampered a detailed functional analysis and limited our knowledge of these dendritic cells (DCs). OBJECTIVE: We studied FcepsilonRI-mediated mechanisms of LCs and IDECs with the help of a novel in vitro model. METHODS: Langerhans cell-like dendritic cells (LC-DCs) and inflammatory dendritic epidermal cell-like dendritic cells (IDEC-DCs) bearing FcepsilonRI have been generated from monocytes of the same atopic donor and compared functionally with LCs and IDECs isolated from the skin of patients with AD. RESULTS: We found that FcepsilonRI-activated LC-DCs release chemotactic signals, and supernatants of FcepsilonRI-activated LC-DCs increase the migratory capacity of precursor cells of IDECs and naive T cells in vitro. FcepsilonRI-activated IDEC-DCs produce high amounts of proinflammatory cytokines and chemokines and might thereby amplify the inflammatory immune reaction in patients with AD. Furthermore, FcepsilonRI-activated IDEC-DCs prime naive T cells into IFN-gamma-producing T cells and release IL-12 and IL-18, which together might lead to the switch of the initial T(H)2-type immune response into a response of the T(H)1 type in vivo. CONCLUSION: The present study provides evidence that FcepsilonRI-activated LC-DCs and IDEC-DCs contribute distinctly to the outcome of T-cell responses in vitro and might have implications for the biphasic nature of AD in vivo.

Antigen Presentation↗
PubMed1978

Surface membrane changes of T cells induced by syngeneic tumour cells. II. T-cell defects induced by small tumour cell inocula or tumour cell antigens.

Injection of a large number of tumour cells, like other strong immunogenic challenges, is followed within 6 h by the uptake of cytophilic Ig (probably complexes) by a subpopulation of T cells. This phenomenon, known as the "6-hour T-cell response" is abrogated when small tumour cell inocula (10(2)), or small amounts of a preparation from tumour cells, which contains tumour antigens, are injected prior to the immunogenic challenge Abrogation of the "6-hour T-cell response" resulted in a decrease in specific anti-tumour cell immunity as tested in vitro by measuring growth inhibition (cytostasis). It has also resulted in loss of the amplifying function on antibody formation against sheep erythrocytes, normally detected in a T-B cell co-operative system when T cells are used 6 h after priming with sheep erythrocytes. It is postulated that this T-cell defect may represent a mechanism by which tumour cells, in the early stages of their growth, interfere with inductive stages of the immune response for a sufficient period of time to allow the tumour to grow beyond immune control.

Animals↗
PubMed2004

Clusterin expression distinguishes follicular dendritic cell tumors from other dendritic cell neoplasms: report of a novel follicular dendritic cell marker and clinicopathologic data on 12 additional follicular dendritic cell tumors and 6 additional interdigitating dendritic cell tumors.

While tumors of dendritic cell lineage may have overlapping histomorphologic features, most but not all cases can be classified using an immunohistochemical panel, including CD21, CD23, CD35, CD1a, and S-100. Based on observations that clusterin is expressed in benign follicular dendritic cells, clusterin expression in 32 dendritic cell tumors was evaluated. Diffuse strong staining for clusterin was seen in 12 of 12 follicular dendritic cell tumors. Two of these cases were negative for traditional markers (CD21, CD23, CD35); they were classified based on characteristic ultrastructural features. Three of 6 interdigitating dendritic cell tumors were negative for clusterin and 3 showed focal weak positivity. Clusterin staining in Langerhans cell histiocytosis ranged from negative (6 of 14) to weak/moderate (8 of 14). Follicular dendritic cell tumors behaved as benign tumors or low-grade sarcomas. Interdigitating dendritic cell tumors demonstrated a widely variable behavior, ranging from benign to rapidly fatal disease. Based on this initial study, strong clusterin staining supports a diagnosis of follicular dendritic cell tumor. Thus, staining for clusterin is useful in classification of dendritic cell tumors, particularly when the more common markers of follicular dendritic cells are not expressed.

Adolescent↗
PubMed1996

Selectively impaired development of intestinal T cell receptor gamma delta+ cells and liver CD4+ NK1+ T cell receptor alpha beta+ cells in T cell factor-1-deficient mice.

T cell factor-1 (Tcf-1) is a transcription factor that binds to a sequence motif present in several T cell-specific enhancer elements. In Tcf-1-deficient (Tcf-1-/-) mice, thymocyte development is partially blocked at the transition from the CD4-8+ immature single-positive stage to the CD4+8+ double-positive stage, resulting in a marked decrease of mature peripheral T cells in lymph node and spleen. We report here that the development of most intestinal TCR gamma delta+ cells and liver CD4+ NK1.1+TCR alpha beta+ (NK1+T) cells, which are believed to be of extrathymic origin, is selectively impaired in Tcf-1-/- mice. In contrast, thymic and thymus-derived (splenic) TCR gamma delta+ cells are present in normal numbers in Tcf-1-/- mice, as are other T cell subsets in intestine and liver. Collectively, our data suggest that Tcf-1 is differentially required for the development of some extrathymic T cell subsets, including intestinal TCR gamma delta+ cells and liver CD4+ NK1+T cells.

Animals↗
PubMed1992

Recognition of heterogeneous lymphokine-activated killer (LAK) receptors on Kaposi's sarcoma cells, endothelial cells, and monocytes/macrophages: evidence of distinct LAK-cell antigen on Kaposi's sarcoma cells--potential for use of LAK cells for immunotherapy.

The purpose of this study was to determine the potential use of lymphokine-activated killer (LAK) cells against Kaposi's sarcoma (KS) cells. We used chromium release cold-target inhibition assay for understanding the expression of heterogeneous LAK-cell antigens (Ags) on KS cells, endothelial cells (ECs), and monocytes/macrophages (M phi) which could allow for the utilization of LAK-cell immunotherapy in KS without side effects. Our data show that (i) all three cell types express the CD18 Ag of LFA-1 or Leu-CAM, (ii) rare KS cells from eyes cannot cold target-inhibit ECs, (iii) KS cells express a distinct LAK-cell Ag, which we have called LAK-KS Ag, and (iv) LAK-KS Ag allows for cold-target inhibition between different KS cells. The identification of LAK-KS Ag and a monoclonal antibody capable of inhibiting lysis of ECs and M phi without obstructing LAK-KS Ag would be important.

Antigens, CD↗
PubMedDate not supplied

Cell-cell adhesion molecules and their associated proteins in bladder cancer cells and their role in mitogen induced cell-cell dissociation and invasion.

Three bladder cell lines (EJ138, RT112/84 and T24/83) were used to examine the expression of E-cadherin, desmoglein, their associated proteins and their role in cell-cell dissociation and invasion using hepatocyte growth factor/scatter factor (HGF/SF). Both immunocytochemistry and Western blotting revealed that RT112/84 cells expressed high levels of E-cadherin, alpha-, beta-, and gamma-catenins. However, there was no expression of E-cadherin and very low levels of alpha- and beta-catenin expression detected in both EJ138 and T24/83 cells. In contrast, all three cell lines were found to express desmoglein, desmoplakin and c-Met. An in vitro invasion assay showed that both EJ138 and T24/83 cells were highly invasive, however, RT112/84 cells were found to have very limited invasion. Invasion of RT112/84 cells was significantly increased by inclusion of either antibody to E-cadherin or motogen (HGF/SF) in the culture medium. This did not appear to be the case for EJ138 and T24/83 cells. Using immunoprecipitation, HGF/SF induced tyrosine phosphorylation of beta-catenin but not desmoplakin. It is concluded that E-cadherin plays a stronger role than desmosomal cadherin in the control of the in vitro invasion of bladder cancer cells. Activation of beta-catenin and subsequent dysfunction of E-cadherin may be a key mechanism in the induction of invasion by the motogen, HGF/SF.

Animals↗
PubMed1987

Properties of smaller and larger cells from the 16-cell mouse embryo: increase in cell adhesiveness in the smaller cells cultured up to late 16-cell stage.

Blastomeres isolated from 16-cell mouse embryos consist of larger cells and smaller cells. In the intact embryo, the larger cells tend to differentiate to the trophectoderm, while the smaller cells give rise to the inner cell mass. The mode of phenotypic alteration of isolated blastomeres from early 16-cell embryos was examined by culturing them as single cells in vitro. The smaller blastomeres showed an increased tendency to be engulfed, as revealed by aggregation experiments during a 15 h culture period just prior to division into the 32-cell stage, while the larger cells remained showing high engulfing activity during this period. The present result demonstrates that the smaller blastomere continues to adopt a selected differentiation program for a certain period, even after its environment is changed.

Animals↗
PubMed2005

B cells productively engage soluble antigen-pulsed dendritic cells: visualization of live-cell dynamics of B cell-dendritic cell interactions.

Interactions between B lymphocytes and Ag-bearing dendritic cells (DC) likely occur at inflammatory sites and within lymphoid organs. To better understand these interactions we imaged B cells (TgB) from hen egg lysozyme (HEL) transgenic mice and DC pulsed with HEL (DC-HEL) in collagen matrices. Analysis of live-cell dynamics revealed autonomous movements and repeated encounters between TgB cells and DC-HEL that are best described by a "kiss-run and engage" model, whereas control B cells had only short-lived interactions. Ag localized at contact sites between TgB cells and DC-HEL, and both cell types rearranged their actin cytoskeletons toward the contact zone. The interaction of a TgB cell with a HEL-bearing DC triggered strong Ca2+ transients in the B cells. Thus, B cells can productively interact with DC displaying their cognate Ag.

Animals↗
PubMed1986

Characteristics of an established cell line (KU-2) derived from human renal cell carcinoma: I. Cloning of cells and morphological study of clones; II. Cell kinetics of KU-2 cells; III. Detection of type C virus in the culture.

A KU-2 cell line derived from human renal cell carcinoma was established by an indirect culture system using the nude mouse in November, 1976. These cells have been examined from different points of view including light and electron microscopic observation, and chromosomal analysis. Histopathological characteristics of the KU-2 cell line, even after being transplanted back to nude mouse, remain similar. However, the characterization of this established cell line has not been fully elucidated. In the present experiments, attempts have been made to study the cloning of KU-2 cells and morphological feature of clones, cell growth and kinetics, and detection of the type C virus in the culture. These results suggested that the KU-2 cell line was not homogeneous but composed of a heterogeneous population of cells based on morphological difference of 6 clones and discrepancy between population doubling time and generation time when calculated from the growth curve and synchronous culture of the KU-2 cells, which may be explained by the cytotoxic effect of excess thymidine. Also the type C virus was negative in the medium.

Carcinoma, Renal Cell↗
PubMed2001

Interleukin-3 and stem cell factor modulate cell cycle regulatory factors in mast cells: negative regulation of p27Kip1 in proliferation of mast cells induced by interleukin-3 but not stem cell factor.

OBJECTIVE: Interleukin-3 (IL-3) and stem cell factor (SCF) are able to promote survival and proliferation of mast cells. However, the precise signal transduction cascades leading to mast cell proliferation are not clearly understood. Thus, we sought to define the mechanism of mast cell proliferation induced by IL-3 and SCF. MATERIALS AND METHODS: We treated murine bone marrow-derived cultured mast cells (BMCMC) with recombinant IL-3 (rIL-3) or recombinant SCF (rSCF) and examined the effects of rIL-3 and rSCF on cell cycle regulatory factors. RESULTS: Both rIL-3 and rSCF suppressed apoptosis of BMCMC. rSCF induced great proliferation of BMCMC with elevation of the proportions of cells in S and G2/M phases, whereas most BMCMC incubated with rIL-3 were arrested in the G1 phase. The G1/S phase transition is initiated by phosphorylated retinoblastoma protein (pRb), which was prominent in cells stimulated with rSCF. In contrast, rIL-3 relatively increased a dephosphorylated form of pRb in BMCMC. Compared with rIL-3, rSCF induced greater expression of cyclin-dependent kinase (CDK) 2 and CDK4, which are able to phosphorylate pRb, and cyclin D3, a partner of CDK4. BMCMC treated with rIL-3 contained a high amount of a CDK inhibitor p27Kip1 that was suppressed by pretreatment with Ro31-7549, a protein kinase C inhibitor, whereas rSCF induced weak expression of p27Kip1 in BMCMC. CONCLUSION: The results suggest that IL-3 and SCF exert their respective mitogenic effects on mast cells by modulating the expression of pRb, CDK, cyclin, and p27Kip1.

Animals↗
PubMedDate not supplied

Lymphoid cells, small cell lung cancer cells and epithelial cells share a membrane determinant which effects cell proliferation.

Two monoclonal antibodies (mAb) 1D1 and 2A6 were obtained from a fusion following hyperimmunization with prolymphocytic leukaemia (PLL) B cells. These mAb stain a minority of B- and T-cell leukaemias and approximately 20% of peripheral blood and tonsil T and B cells, activated with a variety of mitogens. Interestingly, all small cell lung cancer (SCLC) and bladder carcinoma lines examined were also stained by both mAb. On sections of normal and malignant tissue 1D1 and 2A6 show strong but distinct reactivity with epithelium, and in the case of ID1 staining is also present on endothelial tissue. The addition of purified 1D1 and 2A6 to Epstein-Barr virus (EBV)-transformed B-lymphoblastoid cell lines (B-LCL) and SCLC lines caused a significant increase in the rate of proliferation of these cells. Capping experiments have suggested that these two mAb, despite showing significantly different staining profiles, probably recognize distinct epitopes of the same surface molecule. These studies confirm that a lymphoid-cell associated antigen(s) detected by mAbs 1D1 and 2A6 is expressed on a wide range of normal and malignant cells and related cell lines.

Antibodies, Monoclonal↗
PubMed2001

An obligate role for T-cell receptor alphabeta+ T cells but not T-cell receptor gammadelta+ T cells, B cells, or CD40/CD40L interactions in a mouse model of atopic dermatitis.

BACKGROUND: We recently described a murine model of atopic dermatitis (AD) elicited by epicutaneous sensitization with ovalbumin (OVA). The skin lesions in these mice were characterized by a dermal infiltrate consisting of eosinophils and T cells and by increased expression of the TH2 cytokines IL-4 and IL-5. Epicutaneous sensitization induces a rise in the levels of serum total IgE and OVA-specific antibodies, further indicating that it elicits a predominantly TH2 response. OBJECTIVE: This study was undertaken to assess the roles of T cells, B cells, and CD40L-CD40 interactions in AD. METHODS: Mice with targeted gene deletions were sensitized with OVA. Histologic and immunohistochemical examinations, as well as measurements of IL-4 mRNA, were performed on OVA-sensitized skin. Total and antigen-specific serum IgE levels were determined. RESULTS: RAG2(-/-) mice, which lack both T and B cells, did not exhibit cellular infiltration, induction of dermal IL-4 mRNA, or elevation of serum IgE after OVA sensitization; all of these features were present in B-cell-deficient IgH(-/-) mice. T-cell receptor alpha(-/-) mice did not display cellular infiltration, IL-4 mRNA expression, or increased IgE levels after OVA sensitization, but these responses were elicited in T-cell receptor delta(-/-) mice after sensitization. Absence of CD40 had no effect on these responses. CONCLUSION: These results suggest that alphabeta T cells, but not gammadelta T cells, B cells, or CD40L-CD40 interactions, are critical for skin inflammation and the TH2 response in AD.

Animals↗
PubMed1977

Effect of tumor cells on the generation of cytotoxic T lymphocytes in vitro. I. Accessory cell functions of mouse tumor cells in the generation of cytotoxic T lymphocytes in vitro: replacement of adherent phagocytic cells by tumor cells or 2-mercaptoethanol.

In agreement with previous reports, the primary in vitro response to alloantigens has been shown to be dependent on the presence of macrophages (Mphs). Splenocytes extensively depleted of adherent phagocytic cells did not generate cytotoxic T lymphocytes, and this activity could be completely restored by small numbers of adherent peritoneal cells (accessory cells). Either P388D1 (Mph-like tumor), P388 ("null" tumor) or P815 (mastocytoma) tumor cells, or 2-mercaptoethanol, could completely replace the accessory function normally mediated by accessory cells. These tumor cells did not non-specifically "enhance" the cytotoxic activity generated with normal nondepleted spleen cells. The restored cultures maintained killing specificity to H-2 targets which was mediated by effector T cells as shown by sensitivity to anti-theta and complement. Therefore, Mphs seem not to be the sole cells capable of mediating an accessory function in a primary response to alloantigens in vitro.

Animals↗