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At least 73 records · Page 4Linked to original sources
PubMed1997

Protein S is inducible by interleukin 4 in T cells and inhibits lymphoid cell procoagulant activity.

Extravascular procoagulant activity often accompanies cell-mediated immune responses and systemic administration of pharmacologic anticoagulants prevents cell-mediated delayed-type hypersensitivity reactions. These observations suggest a direct association between coagulation and cell-mediated immunity. The cytokine interleukin (IL)-4 potently suppresses cell-mediated immune responses, but its mechanism of action remains to be determined. Herein we demonstrate that the physiologic anticoagulant protein S is IL-4-inducible in primary T cells. Although protein S was known to inhibit the classic factor Va-dependent prothrombinase assembled by endothelial cells and platelets, we found that protein S also inhibits the factor Va-independent prothrombinase assembled by lymphoid cells. Thus, protein S-mediated down-regulation of lymphoid cell procoagulant activity may be one mechanism by which IL-4 antagonizes cell-mediated immunity.

Animals↗
PubMed1983

Ia-restricted interaction between normal lymphoid cells and SJL lymphoma (RCS) leading to lymphokine production. I. Enhancement and suppression of antibody formation to TI antigens by supernatants and cells from cocultures of RCS and lymphoid cells.

Addition of gamma-irradiated reticulum cell sarcoma (RCS) cells causes suppression of the antibody response to trinitrophenyl (TNP)-keyhole limpet hemocyanin (KLH)-primed syngeneic SJL spleen cells to TNP-polyacrylamide (PAA) in vitro. The response of anti-brain antigen (BAT) + C-treated spleen cells is not suppressed by gamma-RCS, but is suppressed by cells from 48-hr SJL lymph node or thymus + gamma-RCS cultures. Addition of as few as 2.5 x 10(5) cultured (anti-I-A + C treated to remove gamma-RCS) cells causes significant inhibition of the responses of both syngeneic and allogeneic spleen cells. Treatment of gamma-RCS-induced suppressor cells with anti-BAT + C reduces their suppressive activity. In contrast to the cells, supernatants (SN) from (lymph node (LN) + gamma-RCS) cultures greatly enhance, in an antigen-dependent fashion, the responses of untreated or anti-BAT + C-treated Sephadex G10-passed spleen cells to TNP-PAA. TNP-SIII polysaccharide, or TNP-Ficoll, but not as much to TNP-KLH. Addition of SN as late as Day 3 of culture still causes about half as much enhancement as leaving SN in throughout the culture period, but it has no effect if left with the spleen cells for only the first day of culture. SN contains high levels of IL-2 and IFN-gamma; absorption with cells from an IL-2-dependent cytotoxic T-cell line removes the enhancing activity, while treatment with pH 2 to remove the IFN-gamma has no effect. SN from an IL-2-producing T-cell line (LBRM-33) has a similar effect on antibody production to TI antigens as does SN of (LN + gamma-RCS). The results suggest a marked dependency of PFC responses to TI antigen on IL-2 in all strains examined, including SJL, LAF1, DBA/2Ha, and CBA/N, probably through a direct activation of B cells. The findings also suggest that suppressor T cells, induced by gamma-RCS in syngeneic lymphoid cells, absorb the IL-2 needed for responses to TI antigens in vitro.

Animals↗
PubMed1982

Multiple immunoglobulin heavy-chain gene transcripts in Abelson murine leukemia virus-transformed lymphoid cell lines.

Lymphoid cells transformed by Abelson murine leukemia virus (A-MuLV) contain three classes of RNA transcripts from immunoglobulin mu genes. P mu-mRNAs (productive) correspond to the normal 2.7-kilobase (kb) membrane (mu m) and 2.4-kb secreted (mu s) mu mRNA species both in size and coding capacity and occur at approximately equal abundance in most mu-positive (pre-B-like) A-MuLV transformants. A mu-mRNAs (aberrant) generally fall into one of two categories--aberrantly small 2.3-kb mu m and 2.0-kb mu s mRNAs which encode aberrantly small mu polypeptide chains, or normal-sized, V H-containing mu RNAs which do not encode immunologically identifiable mu polypeptide chains. In one case, the latter type of A mu-mRNA was demonstrated to result from an in-phase termination codon in the D segment of the mu mRNA. Also, most, if not all, A-MuLV transformants express members of a 3.0 to 1.9-kb set of C mu-containing, but V H-negative S mu-RNAs (for sterile), the expression of which may occur simultaneously with but independently of P mu-mRNAs or A mu-mRNAs. The S mu-RNA sequences do not encode immunologically identifiable mu chains and can be produced by cells with unrearranged heavy-chain alleles, such as T-lymphocytes, although the structure of the S mu-RNAs from T-lymphoid cells appears to be different from that of B-lymphoid cell S mu-RNAs. Certain A-MuLV transformants also express gamma-RNA sequences that are probably analogous to the three different forms of mu RNA. These data support the concept that heavy-chain allelic exclusion, like that of light chains, is not mediated by control at the DNA or RNA levels but is probably a consequence of feedback control from cytoplasmic mu chains.

Abelson murine leukemia virus↗
PubMed1977

The effect of cell synchronization upon the detection of T and B lymphoid cell receptors on two continuous lymphoid cell lines.

In the present study, the effect of the cell synchronization on the detection of T and B cell surface markers of two continuous lines of lymphoid cells (FL-74 and CT45-S) was examined. Suspension cultures were synchronized by deprivation of isoleucine and surface markers were quantitated by T rosette formation with guinea pig erythrocytes (E) and B rosette formation with an erythrocyte-antibody-complement (EAC) complex. After 24 hr, cells were resuspended in complete culture medium. Virtually 100% of FL-74 cells expressed the T cell marker at time 0, with a progressive decline to 80% at saturation density. A bell-shaped curve for expression of the EAC marker on CT45-S cells was seen with maximum expression in the logarithmic phase of the growth cycle. Spent culture medium was examined for the presence of free soluble receptor. Preincubation of E and EAC in appropriate old medium resulted in 42% inhibition of E rosettes and 42% inhibition of EAC rosettes with FL-74 and CT45-S cells, respectively. Thus quantitation of lymphocyte subpopulations as B, T or null cells with these cellular markers may be influenced by the age of the cell examined, phase of the cell cycle and the amount of free receptor present in the surrounding medium.

B-Lymphocytes↗
PubMed1997

Advanced glycosylated end products activate the functions of cell adhesion molecules on lymphoid cells.

It has been proposed that advanced glycosylated end products (AGEs) are involved in the pathogenesis of vascular damages in both type 1 and type 2 diabetes. Furthermore, it has been assumed that AGEs cause an alteration of both expression and activity of cell adhesion molecules which are responsible for migration of circulating cells through the endothelial layer of the vessels. The effect of AGEs on the activity of cell adhesion molecules was studied in our experiments using the homotypic adhesion assay, specific monoclonal antibodies and lymphoid cell lines. It was shown that proteins glycosylated in vitro seemed to increase the percentage of homotypic aggregation of lymphoid cells. This effect was mediated via the interaction between LFA-1 and ICAM-1 which was demonstrated by the fact that specific monoclonal antibodies against these cell adhesion molecules could block the effect of the AGEs. The results obtained reveal that the advanced glycosylated end products activate the function of cell adhesion molecules on lymphoid cells. It can be speculated that the activation of cell adhesion molecules might enhance the direct cellular contacts between the lymphoid cells in the immune response. Moreover, the effect of AGEs might be responsible for an enhanced adhesion of monocytes to endothelial cells and their migration through the vessel wall.

Antibodies, Monoclonal↗
PubMed1986

High-level expression of the Epstein-Barr virus EBNA1 protein in CV1 cells and human lymphoid cells using a SV40 late replacement vector.

To construct a recombinant plasmid designed to yield large amounts of the Epstein-Barr virus (EBV) nuclear antigen, EBNA1, the EBV BamHI-K fragment (B95-8 strain) was inserted into an expression vector composed of SV40 and pBR322 DNA. The vector replicates in both Escherichia coli and eukaryotic cells. Introduction of such a BamHI-K-containing vector into CV1 monkey cells (using DEAE-dextran, glycerol and chloroquine diphosphate) gave high yields of the correct size EBNA1 protein in 40-50% of the transfected cells. Maximal amounts of EBNA1 could be extracted from the cells at 65-72 h post transfection. Using a quantitative ELISA assay, it was estimated that transfected cells express 500-1000 times more EBNA1 than lymphoid cells, latently infected with EBV. A monoclonal antibody directed against EBNA1 immunoprecipitated two proteins of 74 and 62 kDa from transfected cells. These same two proteins were detected in immunoprecipitation and immunoblot experiments using human EBV-positive polyclonal serum, although this serum also detected several other protein products in transfected cells. In vivo labelling of transfected cells with [32P]orthophosphate showed that the 74- and 62-kDa proteins are modified by phosphorylation. The same vector construction was also used to transfect an EBV-negative human lymphoblastoid cell line (Ramos). Expression of the EBNA1 protein was obtained in up to 20% of the cells.

Animals↗
PubMed1991

Rapid accumulation of measles virus leader RNA in the nucleus of infected HeLa cells and human lymphoid cells.

The 3' terminus of the single-stranded, negative-sense genome of the measles virus comprises a 55-nucleotide-long sequence, which is transcribed into a short, positive-sense RNA called the leader sequence. In other viral systems, this RNA has been shown to modulate host cell transcription. Here, we report the presence of measles virus leader RNA in both cytoplasmic and nuclear fractions of infected HeLa cells as well as T- and B-lymphoid cells. A sharp and rapid increase in the concentration of leader RNA in the nucleus of infected HeLa cells was also observed. The presence and accumulation of leader RNA in the nucleus of infected cells supports the hypothesis that the leader RNA plays a role in the down regulation of host cell transcription and may be responsible for the suppression of immunoglobulin synthesis by measles virus-infected B cells. Such alterations in immune responsiveness could aid in the establishment of a persistent infection by measles virus.

Base Sequence↗
PubMed1979

Mouse erythrocyte rosette formation by human lymphoid cell lines.

Lymphoid cell lines have been studied with respect to mouse erythrocyte rosette formation, a marker for B cells. Cells from six B-cell lines out of fifteen tested were able to form mouse erythrocyte rosettes. When this capacity was studied after neuraminidase pretreatment of the cells, it defined three groups of B lymphoid cell lines according to their reactivity. However, these groups could not be correlated to any of the other B-cell markers, and especially mouse erythrocyte rosette formation appeared unrelated to the class of the immunoglobulin present on the cell surface. Non B-cell lines were never found to form such rosettes. The capacity of B-cell lines to form mouse erythrocyte rosette was further demonstrated to be relatively insensitive to trypsin treatment, and results are presented suggesting some degree of cell cycle dependency of the expression of this marker.

B-Lymphocytes↗
PubMed1990

Reversible G1 arrest in the cell cycle of human lymphoid cell lines by dimethyl sulfoxide.

Proliferation of human B- and T-lymphoid cell lines including Raji and Akata cells was found to be arrested at the G1 stage in the cell cycle by dimethyl sulfoxide (DMSO). The G1 arrest by DMSO occurred gradually and was completed within 96 h after addition of 1.5% DMSO concomitantly with a decrease in growth rate. Progression of G1-phase cells containing a larger amount of RNA into S-phase began 9-12 h after removal of DMSO. At 24 h, the DNA pattern of the cell cycle was similar to that of nontreated log-phase cells. The expression of six differentiation markers on the lymphoid cells was not appreciably changed by treatment with DMSO. On the other hand, the expression of transferrin receptor (one of the growth-related markers) on G1-phase cells 96 h after addition of DMSO was decreased to one-fourth that on log-phase cells and was completely restored 24 h after removal of DMSO. These results indicate that DMSO, known as an inducer of differentiation in several myeloid cell lines, acts as an agent inducing G1 arrest in the cell cycle of the lymphoid cells.

B-Lymphocytes↗
PubMed1979

In situ lymphoid cells of mouse mammary tumors. IV. Comparison of functional activity of lymphoid cells separated from mammary tumors to that of spleen and lymph node cells of tumor-sensitized mice.

Lymphoid cells isolated form several types of mouse mammary tumors are capable of stimulating tumor cell growth or survival in MCT assays. Lymph node and spleen cells of mice bearing such a tumor are specifically cytotoxic to the tumor cells. Surgical removal of the tumor is followed in 4 to 7 days by the appearance of stimulatory capacity in spleens and lymph nodes. By day 10, cytotoxic cells specific for the sensitizing tumor are again detected. These reach a peak on day 13. By day 17 no reactivity is detectable. The functional distribution of tumor-reactive lymphoid cells is different between tumor masses and peripheral lymphoid organs.

Animals↗
PubMed1989

Intercellular contacts between germinal center cells. Mechanisms of adhesion between lymphoid cells and follicular dendritic cells.

Intercellular connections exist between germinal center cells especially between lymphoid cells and follicular dendritic cells (FDC). Even after isolation, FDC remain associated to lymphocytes and are able, in a cell suspension, to establish new connections with others. Using human tonsillar cells or mouse lymph node cells we analysed these connections which were shown to be species-specific. Low temperature as well as absence of Ca++ and Mg++ in the culture medium reduced the adherence of fluorochrome-labeled lymphoid cells to FDC. Colchicine treatment did not impair the adherence, whereas cytochalasin B dit it; this was the first observation underlining the importance of microfibrils in FDC. Antibodies directed towards integrin molecules (LFA-1 alpha or beta chain, CD11a and CD18 respectively) reduced the adherence, others (anti-CR3 or anti-gp 150/95, CD11b and c respectively) did not influence it. Antibodies directed against MHC class II exerted no inhibitory action on the lymphoid cell adhesion to FDC. As, at ultrastructural level, gold-labeled immune complexes can be found between FDC and lymphoid cells, we examined the effect on cell adhesion of the addition of immune complexes to the cell suspensions. It only impaired the lymphoid cell adhesion when complement components were present. IgM complexes were then more inhibitory than IgG complexes. When antibodies against Fc IgG receptors (CD16) were added, the adhesion was strongly reduced whereas antibodies to Fc IgE (CD23) receptors had no influence. The antibody DRC1, specifically recognizing an antigen on human FDC reduced the attachment of cells to FDC. This antigen thus seems to play a role in the intercellular contacts; this is the first function ascribed to this FDC specific antigen.

Animals↗
PubMed1975

Hybrid cells, infected with Theileria parva, formed by fusion of hamster and mouse cells with parasitised bovine lymphoid cells.

Bovine lymphoid cells from a culture line parasitised with Theileria parva were fused to mouse heart (MH) and baby hamster kidney (BHK) cells, grown as monolayers, using inactivated Sendai virus. The resultant heterokaryons contained macroschizonts of T parva. Macroschizonts also occurred in cells that apparently contained only BHK or MH nuclei. Parasites underwent varying degrees of development; in some cases microschizonts resulted, and in other cases massive atypical parasite masses were formed. Fusion occurred more readily between hamster and bovine cells than between mouse and bovine cells.

Animals↗
PubMed1964

INVASION AND DESTRUCTION OF HOMOLOGOUS KIDNEY BY LOCALLY INOCULATED LYMPHOID CELLS.

When lymphoid cell suspensions from the spleen, lymph nodes, blood, and thoracic duct of parental strain adult rats were injected beneath the renal capsule of F(1) hybrid hosts, the transferred cells and/or their progeny invaded the underlying renal cortex and destroyed most of the tubules which they surrounded. The immunogenetic conditions under which this reaction was observed defined it as a graft vs. host reaction (GVHR). On the 7th day the GVHRs were histologically similar to primary renal homografts undergoing rejection. Lymphoid cells from donors tolerant to the other parental strain were inactive after transfer to the hybrid, whereas cells from either normal or sensitized donors consistently produced reactions of about equal severity. Lewis lymphoma cells displayed malignant, invasive activity but did not destroy either isologous or homologous tissue, showing that the presence of an infiltrate was not per se sufficient to damage the parenchyma. These observations indicate that the GVHRs were manifestations of the ability of the transferred lymphocytes to enter into a homograft reaction with consequent destruction of renal parenchyma, and support the hypothesis that at least some of the lymphocytes which are seen infiltrating primary homografts are the agents which effect their destruction.

Animals↗
PubMed1975

Induction of Epstein-Barr virus-associated nuclear antigen during in vitro transformation of human lymphoid cells.

Human lymphoid cells isolated from the peripheral blood of adults, from cord blood, and from fetal liver, spleen, bone marrow, and thymus were cultivated with or without a cell-free preparation of Epstein-Barr virus (EBV) with demonstrated transforming activity. The cultures were examined for the EBV-associated nuclear antigen (EBNA) and for transfromation into permanent lymphoblastoid cell lines (LCL). EBNA, seen only in cultures that had received exogenous EBV, was detected between days 1 and 6 after addition of EBV, most frequently on day 3. EBNA-positive cells had a lymphoblastoid appearance. Transformation into established LCL became apparent between days 12 and 19. The addition of pokeweed mitogen to cultures containing EBV enhanced the development of EBNA, whereas phytohemagglutinin or concanavalin A had no such effect. Neither EBNA nor transfomration was observed in lymphoid cells from fetal thymus. In fetal spleen, bone marrow, and liver cells, EBV regularly induced EBNA and LCL transformation.

Antigens, Viral↗
PubMed1978

In situ lymphoid cells of mouse mammary tumors. II. The characterization of lymphoid cells separated from mouse mammary tumors.

Lymphoid cells were isolated from mouse mammary tumors by isokinetic gradient centrifugation. theta-bearing and ALS-sensitive cells were always the largest subpopulations found in these tumors. In fractions 4 to 6 from the isokinetic gradient, theta-positive cells ranged from 8 to 46% in autochthonous tumors and 14 to 47% in passaged tumors, and ALS-positive cells ranged from 34 to 46% in autochthonous tumors and 14 to 100% in passaged tumors. SIg-positive cells were only found in occasional tumors and, where present, averaged 2% of the separated population. Fc receptor-bearing cells averaged 15% and phagocytic cells averaged 8% of the cells found in fractions 4 to 6 of the gradient. Occasional ALS-positive and one-third of the Fc receptor-bearing and phagocytic cells also separated in fractions 7 to 10 of the isokinetic gradient. Although the individual tumors were very variable in the proportions of the various lymphoid subpopulations that they contained, this variability was a stable characteristic for at least one passage generation.

Animals↗
PubMed1983

O6-Methylguanine-DNA methyltransferase of human lymphoid cells: structural and kinetic properties and absence in repair-deficient cells.

Human lymphoid cell lines contain a DNA repair enzyme which removes the mutagenic alkylation lesion O6-methylguanine from DNA. The enzyme transfers the methyl group to a protein cysteine residue, generating S-methylcysteine, and is inactivated as a consequence of the reaction. Apparently the methylated enzyme represents a dead-end complex. The transfer reaction is very rapid and is completed in less than 1 min at 37 degrees, but methyl group transfer from single-stranded DNA or heavily damaged DNA is less efficient. The active methyltransferase and the methylated protein both have molecular weights of 21,000 to 22,000, as determined by gel filtration. Lymphoid cell lines proficient in repair of O6-methylguanine in vivo, Mex+, contain 10,000 to 25,000 molecules of the methyltransferase per cell. In contrast, repair-deficient cell lines, Mex-, do not contain detectable amounts of the enzyme. The latter point was verified by applying a partial purification procedure for the enzyme to cell-free extracts from two Mex- cell lines.

Burkitt Lymphoma↗