Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “T cell”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed1977

Growth of cells on solid culture medium. II. Cell physiological data of stationary yeast cells and the initiation of cell cycle in nutrient free buffer solution.

For precise experiments with yeast (or other) cells stationary populations are produced by growth on the surface of a solid nutrient medium. The energy supply to these cells is well known from a former publication. The oxygen supply during growth is analysed here in detail. Different types of cell populations can be produced in this way dependent on the thickness of nutrient medium. If such cells are transferred into a liquid buffer solution cell multiplication can be initiated without any nutrient flux into the cell. This new type of initiation of the cell cycle of G1-cells has to be distinguished from the usual initiation by nutrient supply and from the mechanism of meiotic cell division. The dependence of this cell growth on cell volume, pH-value, oxygen concentration and osmotic pressure is analysed and possibilities to avoid this kind of cell multiplication reaction are discussed.

Cell Cycle↗
PubMed1979

Appearance in confluent vascular endothelial cell monolayers of a specific cell surface protein (CSP-60) not detected in actively growing endothelial cells or in cell types growing in multiple layers.

The formation of a highly organized vascular and corneal endothelial cell monolayer is associated with the appearance of a 60,000-dalton cell surface protein (CSP-60) (30,000 daltons after reduction with dithiothreitol) which is not detectable in rapidly growing endothelial cells and in subconfluent cultures that do not yet exhibit the strict morphology of a confluent monolayer. It is also absent from vascular smooth muscle cells and from endothelial cultures that are maintained in the absence of fibroblast growth factor and grow on top of each other at confluence. After disorganization of cells in a confluent endothelial monolayer by urea, EDTA, or trypsin, CPS-60 is no longer exposed on the cell surface, but it reappears as soon as the cells readopt their characteristic two-dimensional configuration. This reorganization can be achieved in the presence of cycloheximide and despite removal of fibronectin by urea, EDTA, or trypsin. Maximal amounts of fibronectin and no CSP-60 are detected in subconfluent, but not yet organized, endothelial cultures or in endothelial cells that no longer form a monolayer of nonoverlapping cells at confluence. Likewise, cultures of vascular smooth muscle cells contain fibronectin but no CSP-60. These results suggest that CSP-60, rather than fibronectin, could be involved in the adoption of a monolayer configuration by confluent endothelial cells.

Aorta↗
PubMed1979

The cells involved in cell-mediated and transplantation immunity in the normal outbred rabbit. XIII. The identity of the responder cells and the role of phagocytic cells in the mixed leucocyte culture reaction.

The ability of rabbit spleen cells depleted of thymus, bone marrow or appendix-derived cells to respond in the one-way mixed leucocyte reaction (MLR) has been investigated. The specific subpopulations of lymphoid cells were eliminated by lysis of these cells in the presence of specific antisera and complement. Phagocytic cells (monocytes and heterophils) were removed with a strong magnet after incubation with carbonyl iron particles. The results indicate that the MLR-responding cells are thymus-derived and that neither bone marrow-derived cells nor appendix-derived cells are essential for the blastogenic response following stimulation with allogeneic cells. A minimum number of phagocytic cells is required for a significant response. These cells, however, exhibit a non-specific (accessory) role and can be supplied by either the responding or the stimulating cell population.

Animals↗
PubMed1975

Non-T cell killing of mammary tumor cells by spleen cells: secretion of antibody and recruitment of cells.

Both T cell-mediated killing and non-T cell-mediated killing of target MTV-induced mammary tumor cells can be detected in microcytotoxicity assay tests of spleen cells from mice immunologically responsive to either the histocompatibility antigens or the virus-associated antigens of the target cells. The non-T cell-mediated cytotoxicity is antibody-dependent; otherwise inactive cells (null cells) can be recruited to activity by target cell-specific factors obtained from the supernatant of short-term cultures of sensitized B cells or provided by the introduction of a small number of sensitized B cells to the wells of the assay plate.

Animals↗
PubMed1977

New groups and segregant series among B-cell alloantigens of the Merrit system. A study of leukemia cells, peripheral B cells, and lymphoblastoid cell lines.

On the basis of reactions with a chronic lymphatic leukemia cell panel, evidence for 6 new specificities of the Merrit B-cell alloantigenic system in man is presented, bringing the number of provisionally defined specificities to 19. These can be roughly divided into two segregant series. The system is well represented on both homozygous and heterozygous B-type lymphoblastoid cell lines. In the cell lines some specificities show a suggestive but inexact correlation with HLA-D locus factors. This correlation is represented also on peripheral blood B cells, on the non-T variety of acute lymphatic leukemia cells, and on acute myeloid leukemia cells. Although great similarities exist, each of the cell populations may manifest differences other than or in addition to mere differences in B-cell antigen frequencies.

B-Lymphocytes↗
PubMed1978

T-T-cell interactions during the vitro cytotoxic allograft responses. I. Soluble products from activated Lyl+ T cells trigger autonomously antigen-primed Ly23+ T cells to cell proliferation and cytolytic activity.

Secondary murine cytotoxic T lymphocyte responses from alloantigen-primed T cells can be induced in vitro by apparently unrelated regimens, such as addition of either concanavalin A (Con A), conditioned medium from Con A stimulated lymphocyte cultures, conditioned medium from secondary mixed lymphocyte cultures (MLC), or stimulator cells sharing only the I-region with the stimulating cells used for primary sensitization. We now report that upon polyclonal (Con A), or antigen-specific (MLC) stimulation, Lyl+ T cells release a factor, which in turn triggers alloantigen primed Ly23+ T cells to proliferation and cytolytic activity. The secondary cytotoxic T lymphocyte inducing factor (SCIF) is produced within 24 h. For its production, an intact protein metabolism, not DNA metabolism, is required. Once induced, the functional activity of SCIF is nonspecific and not H-2 restricted. SCIF allows exponential growth and long-term propagation of cytolytic Ly23+ T cells with specificity to alloantigens used for primary sensitization. SCIF induced activation of alloantigen primed Ly23+ T cells does not require the presence of alloantigens. The results therefore reveal a process by which Lyl+ T-cell-derived nonspecific factor(s) induce autonomously Ly23+ T-cell-mediated, antigen-specific, cytotoxic T lymphocyte responses.

Animals↗
PubMed1977

Heterogeneity of B cells reacting with T-cell factors. Evidence for matching T-cell and B-cell subsets.

Spleen T cells have been stimulated with Concanavalin A (Con A) under conditions which lead to the production of non-specific factor (NSF), a substance which replaces T cells for B-cell responses to certain antigens. We have examined the ability of multiple aliquots of B cells to react to the NSF derived from single T cells, and have found great heterogeneity of response. We postulate that there exist subsets of T cells which vary in either the quantity or the quality of the non-specific factor(s) they can produce on stimulation, and that in turn there must also be matching subsets of B cells which may vary in their susceptibility to such factors.

Animals↗
PubMed1978

Islet cells as a component of pancreatic ductal neoplasms. I. Experimental study: ductular cells, including islet cell precursors, as primary progenitor cells of tumors.

The ductular complex of the Syrian hamster pancreas represents a system of conduit which encompasses intercalated (intralobular), periinsular, and intrainsular ductules. The intercalated (intralobular) ductules comprise centroacinar and intercalated cells. A meshwork of small ductules (invisible by usual histologic procedures) surrounds islets (periinsular ductules) and extends in the form of often ramified tiny channels within the islet (intrainsular ductules). Although the function of the latter ductules is obscure, their cells seem to make up one of the undifferentiated cellular units of the pancreas, and as such are also the progenitors of beta-cells of the islets (islet cell precursor = IP). Systematic histologic examination of the pancreas in this species treated with pancreatic carcinogen N-nitrosobis(2-oxopropyl)amine indicated that ductular cells, especially those of periinsular and intrainsular origin, are the most responsive to this carcinogen. The neoplastic process was initiated with hyperplasia of intercalated (intralobular) ductular and interlobular ductal cells associated with newly formed islets (nesidioblastosis). This process was followed by excess formation of mature but especially of immature islet cells and their precursors (IP) in the islet periphery, as well as with the appearance, distention, and multiplication of periinsular and particularly of intrainsular ductules. The hyperplasia, metaplasia, and malignant alteration of these periinsular and intrainsular ductules (including IP) and, to a lesser degree, of intercalated ductules indicated their histogenetic relationship and their potency for reproducing embryonic tissue on carcinogenic stimulus. The similarity of some induced lesions to diabetes has been emphasized.

Animals↗
PubMed1979

Teratocarcinoma stem cells have a cell surface carbohydrate-binding component implicated in cell-cell adhesion.

Teratocarcinoma stem cells maintained in the undifferentiated state express a carbohydrate-binding component that recognizes oligomannosyl residues. This cell surface molecule is detected by a rosetta assay in which the stem cells form rosettes with glutaraldehyde-fixed trypsinized rabbit erythrocytes. Addition of simple sugars to the assay mixture has little effect, but rosette formation is inhibited by a series of mannose-rich glycoproteins (yeast invertase, yeast mannans and horseradish peroxidase). Periodate oxidation eliminates the inhibitory activity of invertase whereas pronase digestion has little effect, indicating that carbohydrate moieties are essential for inhibition. Invertase and its glycopeptide derivatives also inhibit the reaggregation of dispersed stem cells and promote the dissociation of preformed aggregates. These results suggest that intercellular adhesion of teratocarcinoma stem cels may be the consequence of the interaction of a lectin-like component detected in the rosette assay with a complementary oligosaccharide receptor on adjacent cells.

Animals↗
PubMed1979

Mechanochemical proteins, cell motility and cell-cell contacts: the localization of mechanochemical proteins inside cultured cells at the edge of an in vitro "wound".

We have examined the distribution of several mechanochemical proteins inside rat A10 cells in monolayer culture, both in sparse cultures and at the edges of in vitro "wounds" in confluent cultures. The proteins examined were actin, myosin, tropomyosin, alpha-actinin, filamin, and tubulin. In each experiment, a pair of these proteins (one of which was usually actin) were examined simultaneously by double fluorescence staining methods. Actin was specificially stained by double fluorescence staining methods. Actin was specifically stained by a method based on heavy meromyosin binding, while the other proteins were specifically stained by indirect immunofluorescence procedures. The most important of the various results described was obtained with cells moving out from the edge of an in vitro wound. Within the flat leading lamella of such a cell, there was an extended region in which myosin was severely depleted or absent compared to the proximal regions of the same cells. By contrast, the other proteins were abundantly present throughout the leading lamella, except for tropomyosin, which was somewhat depleted but not as extensively as myosin. In Nomarski optics, there was no detectable morphological differentiation between the region depleted of myosin and the more proximal portion of the same lamella. While the depletion of myosin from the motile regions of cells does not rule out the involvement of some form of an actomyosin sliding filament mechanism, it suggests that other molecular mechanisms for generating motility be seriously considered.

Actinin↗
PubMed1975

Somatic cell hybrids between mouse peritoneal macrophages and simian-virus-40-transformed human cells: II. Presence of human chromosome 7 carrying simin virus 40 genome in cells of tumors induced by hybrid cells.

Cells derived from tumors induced in "nude" mice after injection of cells that were hybrids between mouse peritoneal macrophages and simian virus 40 (SV40)-transformed human cells were found to retain the human chromosome 7 carrying the SV40 genome, and indicate that the presence of human chromosome 7 carrying the SV40 genome is responsible for the expression of the tumorigenic phenotype in the hybrid cells.

Animals↗
PubMed1978

Corynebacterium parvum-induced peritoneal exudate cells with rapid cytolytic activity against tumour cells are non-phagocytic cells with characteristics of natural killer cells.

Peritoneal exudate cells taken from mice 3 days after intraperitoneal treatment with Corynebacterium parvum (Cp) have been shown to kill specifically certain tumour targets in vitro. We have analysed in detail such Cp-induced cytotoxic cells as to their cellular characteristics, considering the fact that size and charge characteristics of cellular subgroups are useful markers in describing their representative characteristics. We could thus show that the cytolytic cell could not be classified as a macrophage. They behaved, in every manner analysed, exactly as the previously defined natural killer cells found in the lymphoid organs of normal mice.

Animals↗
PubMed1979

Cellular and genetic control of antibody responses. V. Helper T-cell recognition of H-2 determinants on accessory cells but not B cells.

Requirements for helper T-cell recognition of H-2 determinants expressed on adherent accessory cells and on B cells was individually assessed in the anti-hapten PFC responses to TNP-KLH. Complicating allogeneic effects were minimized or avoided by the use of helper T cells from normal F1 hybrids, parent leads to F1 chimeras, and F1 leads to parent chimeras. The results of both in vitro and in vivo experiments demonstrated that: (a) helper T cells are not required to recognize the identical H-2 determinants on both accessory cells and B cells; (b) helper T cells are required to recognize K or I-A region-encoded determinants expressed on accessory cells; (c) no requirement was observed in vitro or in vivo for helper T-cell recognition of B-cell-expressed H-2 determinants; and (d) no requirement was observed for H-2 homology between accessory cells and B cells. The absence of required helper T-cell recognition of the identical H-2 determinants on both accessory cells and B cells was demonstrated in two ways: (a) naive of KLH-primed (A x B)F1 hybrid helper T cells collaborated equally well with B cells from either parentA or parentB in the presence of accessory cells from either parent; (b) A leads to (A x B)F1 chimeric spleen cells depleted of accessory cells collaborated equally well with accessory cells from either parentA or parentB, even though the B cells only expressed the H-2 determinants of parentA. A requirement for helper T-cell recognition of K or I-A region-encoded H-2 determinants on accessory cells was also demonstrated in two ways: (a) (A x B)F1 leads to parentA chimeric spleen cells depleted of accessory cells collaborated with accessory cells from parentA but not parentB; and (b) (A x B)F1 leads to parentA chimeric helper T cells collaborated with normal F1 B cells only in the presence of parental or recombinant accessory cells that expressed the K or I-A region-encoded determinants of parentA. Although restricted in their ability to recognize H-2 determinants on accessory cells, it was demonstrated both in vitro and in vivo that (A x B)F1 leads to parentA chimeric helper T cells were able to collaborate with B cells from either parentA or parentB. In vitro in the presence of accessory cells from parentA, (A x B)F1 leads to parentA chimeric helper T cells collaborated equally well with B cells from either parent. In addition, the inability of (A x B)F1 leads to parentA chimeric helper T cells to collaborate with (B + accessory) cells from parentB was successfully reversed by the addition of parentA SAC as added accessory cells. In vivo, upon the addition of parentA accessory cells, (A x B)F1 leads to parentA chimeric helper T cells collaborated with parentB B cells in short-term adoptive transfer experiments.

Animals↗
PubMed1975

Phagocytosis of lymphoblastoid cells and cell destruction of human malignant tumor cells.

On the basis of the previous study, on the cell interaction between malignant tumor cells and other cells, especially with lymphocytes, the present study was carried out by investigating cell to cell interaction of human malignant tumor cells and human lymphoblastoid cells such as T-cell (MOLT-4 cell) and B-cell (Burkitt lymphoma cell). As a result it has been revealed that live lymphoblastoid cells were not adhered on the cell surface of the tumor cells, nor is it ingested by tumor cells, but in thepresence of HVJ (Sendai virus: 2,000 H.A. units) it adheres slightly on the cell surface of tumor cell but no cell fusion of tumor cells and lymphoblastoid cells is observable. On the other hand, the tumor cell as well as T-cell and B-cell all have receptors to concanavalin A (Con. A) on their cell surfaces, and they show a marked cell binding such as tumor cell and T-cell, tumor cell and B-cell, and there can be observed a marked phagocytosis of lymphoblastoid cells by tumor cells. Moreover, the tumor cells that have phagocytized lymphoblastoid cells undergo a marked cell destruction within 4 hours of cell-binding and phagocytosis, which is especially prominent in the case of phagocytosis of E.B cell by tumor cell.

Animals↗
PubMed1979

Modulation by thymus-derived (T) cells of thyroid cell-stimulated prostaglandin E release by human peripheral blood mononuclear cells.

Cultures of plastic-adherent, human peripheral blood mononuclear cells generated prostaglandin E (PGE). Culture of the adherent cells (predominantly monocytes) with human thyroid cells enhanced PGE accumulation in the medium, although to a lesser degree than occurs with unseparated blood mononuclear cells. Recombination of the adherent cells with monocyte-depleted, nonadherent cells restored both basal and thyroid cell-stimulated PGE generation to the levels seen with unseparated cells. Thymus-derived (T) cells, obtained by rosetting with sheep erythrocytes, similarly enhanced both the adherent cell basal PGE production as well as the increased PGE accumulation that occurs in the presence of thyroid cells (50-120% augmentation by the T cells). Significant augmentation of thyroid cell-stimulated PGE release by 10(5) adherent cells occurred with the addition of as few as 5 x 10(4) T cells. Culture medium transfer experiments and separation of cell types during culture by a semipermeable membrane provided evidence against the possibility that the adherent cells were releasing a factor that stimulated T-cell PGE generation or that T cells were releasing a factor that enhanced adherent cell PGE generation. The results suggest instead that this T-cell effect requires direct contact with the adherent cells. These data demonstrate the importance of human T cells in the release by adherent cells of PGE, a mediator of suppressor function by some immune cells.

Adult↗
PubMed1977

Regulatory functions of hapten-reactive helper and suppressor T lymphocytes. II. Selective inactivation of hapten-reactive suppressor T cells by hapten-nonimmunogenic copolymers of D-amino acids, and its application to the study of suppressor T-cell effect on helper T-cell development.

An experimental condition was established in vivo for selectively eliminating hapten-reactive suppressor T-cell activity generated in mice primed with a para-azobenzoate (PAB)-mouse gamma globulin (MGG)-conjugate and treated with PAB-nonimmunogenic copolymer of D-amino acids (D- glutamic acid and D-lysine; D-GL). The elimination of suppressor T-cell activity with PAB-D-GL treatment from the mixed populations of hapten- reactive suppressor and helper T cells substantially increased apparent helper T-cell activity. Moreover, the inhibition of PAB-reactive suppressor T-cell generation by the pretreatment with PAB-D-GL before the PAB-MGG-priming increased the development of PAB-reactive helper T-cell activity. The analysis of hapten-specificity of helper T cells revealed that the reactivity of helper cells developed in the absence of suppressor T cells was more specific for primed PAB-determinants and their cross-reactivities to structurally related determinants such as meta-azobenzoate (MAB) significantly decreased, as compared with the helper T-cell population developed in the presence of suppressor T lymphocytes. In addition, those helper T cells generated in the absence of suppressor T cells were highly susceptible to tolerogenesis by PAB-D- GL. Similarly, the elimination of suppressor T lymphocytes also enhanced helper T-cell activity in a polyclonal fashion in the T-T cell interactions between benzylpenicilloyl (BPO)-reactive T cells and PAB- reactive T cells after immunization of mice with BPO-MGG-PAB. Thus inhibition of BPO-reactive suppressor T-cell development by the BPO-v-GL- pretreatment resulted in augmented generation of PAB-reactive helper T cells with higher susceptibility of tolerogenesis to PAB-D-GL. Thus, these results support the notion that suppressor T cells eventually suppress helper T-cell activity and indicate that the function of suppressor T cells related to helper T-cell development is to inhibit the increase in the specificity and apparent affinity of helper T cells in the primary immune response. The hapten-reactive suppressor and helper T lymphocytes are considered as a model system of T cells that regulate the immune response, and the potential applicability of this system to manipulating various T cell-mediated immune responses is discussed in this context.

Animals↗