scholarly journals Macrophage plasminogen activator: induction by products of activated lymphoid cells.

1977 ◽  
Vol 145 (2) ◽  
pp. 429-437 ◽  
Author(s):  
J D Vassalli ◽  
E Reich
Keyword(s):  
Cell Migration ◽  
Conditioned Medium ◽  
Plasminogen Activator ◽  
Cell Types ◽  
Enzyme Synthesis ◽  
Hormonal Control ◽  
Lymphoid Cells ◽  
Spleen Cells ◽  
Con A ◽  
By Products

Macrophages obtained from the peritoneal cavity of untreated mice do not ordinarily synthesize plasminogen activator. However, induction of enzyme synthesis and secretion occurs when such macrophages are cultured in presence of conditioned medium from Con A-stimulated spleen cells. Plasminogen activator production by macrophages from endotoxin or thioglycollate medium-injected mice, which spontaneously secrete substantial amounts of the enzyme, is also markedly increased in presence of such conditioned medium. These results suggest that macrophage plasminogen activatory production may be regulated in part by lymphocytes. They provide further evidence to link macrophage plasminogen activator with cell migration and inflammation, and also support the view that in macrophages, as in certain other cell types, synthesis and secretion of this enzyme are under hormonal control.

scholarly journals POTENTIATION OF THE T-LYMPHOCYTE RESPONSE TO MITOGENS

1972 ◽  
Vol 136 (1) ◽  
pp. 128-142 ◽  
Author(s):  
Igal Gery ◽  
Richard K. Gershon ◽  
Byron H. Waksman
Keyword(s):  
T Lymphocyte ◽  
Blood Cells ◽  
Human Peripheral Blood ◽  
Lymphoid Cells ◽  
Spleen Cells ◽  
Lymphocyte Response ◽  
Con A ◽  
Visible Effect ◽  
Pha Response ◽  
Human And Mouse

Human and mouse lymphoid cells, stimulated by phytohemagglutinin (PHA) or lipopolysaccharide W (LPS), release supernatant factor(s) which are mitogenic for mouse thymocytes and which potentiate their responses to PHA or concanavalin A (Con A), The term LAF (lymphocyte-activating factor) is proposed for this activity. LAF not only enhances the mitotic responses of the less dense thymus subpopulations (A, B, and C) separable on discontinuous bovine serum albumin (BSA) gradients but also gives substantial responses in the otherwise inert cells of the denser fractions D and P. LAF does not exert a potentiating stimulatory effect on the responses of unfractionated mouse spleen cells, but does act synergistically with PHA on nonadherent spleen cells and on spleen cells of mice of several strains 5 days after irradiation and injection of thymocytes. Similarly LAF, which has no visible effect on unfractionated human peripheral blood cells, strongly potentiates the PHA response of column-purified lymphocytes, when these are cultured at low concentration. We conclude that LAF stimulates both central and peripheral T lymphocytes and enhances their responses to other stimulants.

Plasma membrane mediated thymidine transport in AKR spleen cells

1980 ◽  
Vol 58 (12) ◽  
pp. 1405-1413 ◽  
Author(s):  
Phyllis R. Strauss ◽  
James M. Sheehan ◽  
Judith Taylor
Keyword(s):  
Inbred Mouse ◽  
Lymphoid Cells ◽  
Time Dependent ◽  
Transport Systems ◽  
Mouse Strains ◽  
Spleen Cells ◽  
Con A ◽  
Thymidine Transport ◽  
Akr Mice

In this paper we characterize the thymidine transport systems in nonadherent spleen cells from normal leukemic (AKR) mice and from AKR mice which have been stimulated in vivo with concanavalin A (Con A). We have shown that splenic lymphocytes from normal AKR mice transport thymidine (two kinetic components, Km values of 34 μM and 1.6 mM) whereas lymphoid cells from C57L/J and outbred (CD-1) mice do not. Following Con A stimulation of AKR mice, three components (Km values of 6 μM, 212 μM, and millimolar range) were observed. The current data should be compared with previously published results for splenocytes from Con A stimulated CD-1 mice. Although those cells transport thymidine with two kinetic components (Km values of 160 μM and 4 mM), they lacked the lowest Km system present in AKR splenocytes.Thymidine transport was also examined in lymphocytes from several AK × L recombinant inbred mouse strains derived from the cross AKR/J × C57L/J. Two strains which lacked MuLV did not show time-dependent thymidine translocation whereas two strains which possessed MuLV demonstrated time-dependent thymidine translocation. Moreover, cells from the congenic strain L.AKR-Akv-2, which carried the Akv-2 genome on a C57L background, also showed thymidine transport. Thus a unique ability to transport thymidine can be correlated with the presence of the murine leukemia virus genome.

scholarly journals Separation of helper and suppressor T lymphocytes on a ficoll velocity sedimentation gradient.

1976 ◽  
Vol 143 (5) ◽  
pp. 1199-1210 ◽  
Author(s):  
H Tse ◽  
R W Dutton
Keyword(s):  
T Cells ◽  
Cell Types ◽  
Velocity Sedimentation ◽  
Constant Number ◽  
Spleen Cells ◽  
Suppressor T Cells ◽  
Con A ◽  
Normal Spleen ◽  
Suppressor T Lymphocytes

A 5-20% Ficoll velocity sedimentation gradient has been successfully applied to separate concanavalin A (Con A)-induced helper; and suppressor T cells. When titrated into a constant number of fresh normal spleen cells responding to sheep erythrocytes, cells from the top pool show stimulatory effects while those from the bottom pool show inhibitory activity. Both activities are found to be Con A dependent and anti-theta sensitive. We conclude that Con A-induced helper and suppressor T cells are distinct subpopulations and such separation will allow further characterization of these cell types.

scholarly journals Regulatory mechanisms in cell-mediated immune responses. IV. Expression of a receptor for mixed lymphocyte reaction suppressor factor on activated T lymphocytes.

1976 ◽  
Vol 144 (5) ◽  
pp. 1214-1226 ◽  
Author(s):  
S S Rich ◽  
R R Rich
Keyword(s):  
T Lymphocytes ◽  
Mixed Lymphocyte Reaction ◽  
Suppressor Cell ◽  
Lymphoid Cells ◽  
Resting Cells ◽  
Spleen Cells ◽  
Con A ◽  
Suppressor Activity ◽  
Suppressor Factor ◽  
Genetic Homology

Suppression of the mixed lymphocyte reaction (MLR) by a soluble factor produced by alloantigen-activated spleen cells requires genetic homology between the factor-producing cells and responder cells in MLR. The ability of lymphocytes used as MLR responder cells to adsorb MLR suppressor factor was tested to investigate the expression of a receptor structure for suppressor molecules. Normal spleen or thymus cells had no effect on suppressor activity. Concanavalin A (Con A)-activated thymocytes, however, effectively removed suppressor activity, suggesting that the receptor is expressed only after activation and is not present or not functional on resting cells. Significantly neither phytohemagglutinin- nor lipopolysaccharide-activated lymphoid cells absorbed the factor. Furthermore, only Con A-activated thymocytes demonstrating genetic homology with the cell producing suppressor factor for H-2 regions to the right of I-E were effective absorbants. Alloantigen-stimulated spleen cells syngeneic to the suppressor cell also removed suppressor activity. These data support an hypothesis that subsequent to stimulation in MLR, T lymphocytes express a receptor, either through synthesis or alteration of an existing molecular structure, which then provides the appropriate site for interaction with suppressor molecules.

scholarly journals Synergy between adjuvant arthritis and collagen-induced arthritis in rats.

1985 ◽  
Vol 162 (3) ◽  
pp. 962-978 ◽  
Author(s):  
J D Taurog ◽  
S S Kerwar ◽  
R A McReynolds ◽  
G P Sandberg ◽  
S L Leary ◽  
...  
Keyword(s):  
Adjuvant Arthritis ◽  
Type Ii Collagen ◽  
Passive Transfer ◽  
Lymphoid Cells ◽  
Joint Disease ◽  
Type Ii ◽  
Spleen Cells ◽  
Con A ◽  
Collagen Induced Arthritis ◽  
Immune Effector

Adjuvant arthritis (AA) in rats is susceptible to cell-mediated passive transfer. Collagen-induced arthritis (CIA) in rats is susceptible to passive transfer with antibody to type II collagen. We report here the development of strikingly severe arthritis in Lewis rats as the result of synergy between passively transferred antibody to type II collagen from rats with CIA and concanavalin A (Con A)-stimulated lymph node or spleen cells from syngeneic rats with AA. Similar synergy was seen in rats with AA given anticollagen antibody, in rats with CIA given Con A-stimulated adjuvant spleen cells, and in rats actively immunized with CII and complete Freund's adjuvant. The synergistic process caused a very severe polyarthritis, characterized by marked swelling and erythema in all the joints of the distal extremities, with histologic and radiographic evidence of early, extensive erosion of articular cartilage. Synergy was apparent if the lymphoid cells from AA rats were given up to 1 mo after a single injection of anticollagen antibody. No synergy was seen when normal rat immunoglobulin or anti-ovalbumin antibody was substituted for anticollagen antibody, when Con A-stimulated lymphoid cells from normal rats or donors with CIA were used, or when Con A-stimulated AA lymphoid cells were irradiated before transfer. Synergy between separate immune effector mechanisms may represent a general phenomenon in the pathogenesis of inflammatory joint disease.

scholarly journals SYNERGY AMONG LYMPHOID CELLS MEDIATING THE GRAFT-VERSUS-HOST RESPONSE

1970 ◽  
Vol 131 (2) ◽  
pp. 235-246 ◽  
Author(s):  
Harvey Cantor ◽  
Richard Asofsky
Keyword(s):  
Cell Types ◽  
Lymphoid Cells ◽  
Cell Populations ◽  
Lymphoid Tissues ◽  
Spleen Cells ◽  
F1 Hybrid ◽  
Graft Versus Host ◽  
Adult Mice ◽  
Thymus Cells ◽  
Old Mice

The capacity of cells from different lymphoid tissues obtained from Balb/c mice to produce graft-vs.-host (GVH) reactions was quantitatively determined in C57BL/6N by Balb/c F1 hybrid recipients. Synergistic responses were observed when small numbers of cells from lymphoid tissues that were rich in GVH activity such as spleen and femoral lymph node were combined with weakly reactive thymus cells. Thymus and spleen cells obtained from 1-wk old mice were separately inactive but produced moderate GVH reactions when combined in equal proportions. GVH activity of spleen cells from mice thymectomized at 3 days of age was partially restored by the addition of small numbers of spleen or thymus cells from adult mice. Changes in ratio between the two cell populations markedly affected the degree of synergy. Synergy was not observed when Balb/c cells were combined with Balb/c x C57BL/6N F1 hybrid cells and inoculated into C57BL/6N recipients, but was demonstrated when Balb/c and C57BL/6N cells were combined and inoculated into F1 recipients, indicating that a genetic disposition to mount GVH reactions in both populations is required to produce synergy. The data indicate that at least two cell types are necessary for GVH reactions, and that synergy between cell populations results from favorable adjustments in the ratio between these two cell types.

scholarly journals Selective deletion of SHIP-1 in hematopoietic cells in mice leads to severe lung inflammation involving ILC2 cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xujun Ye ◽  
Fengrui Zhang ◽  
Li Zhou ◽  
Yadong Wei ◽  
Li Zhang ◽  
...  
Keyword(s):  
Lung Inflammation ◽  
Airway Remodeling ◽  
Pulmonary Inflammation ◽  
Hematopoietic Cells ◽  
Cell Lineage ◽  
Allergic Inflammation ◽  
Cell Types ◽  
Lymphoid Cells ◽  
Whole Body

AbstractSrc homology 2 domain–containing inositol 5-phosphatase 1 (SHIP-1) regulates the intracellular levels of phosphotidylinositol-3, 4, 5-trisphosphate, a phosphoinositide 3–kinase (PI3K) product. Emerging evidence suggests that the PI3K pathway is involved in allergic inflammation in the lung. Germline or induced whole-body deletion of SHIP-1 in mice led to spontaneous type 2-dominated pulmonary inflammation, demonstrating that SHIP-1 is essential for lung homeostasis. However, the mechanisms by which SHIP-1 regulates lung inflammation and the responsible cell types are still unclear. Deletion of SHIP-1 selectively in B cells, T cells, dendritic cells (DC) or macrophages did not lead to spontaneous allergic inflammation in mice, suggesting that innate immune cells, particularly group 2 innate lymphoid cells (ILC2 cells) may play an important role in this process. We tested this idea using mice with deletion of SHIP-1 in the hematopoietic cell lineage and examined the changes in ILC2 cells. Conditional deletion of SHIP-1 in hematopoietic cells in Tek-Cre/SHIP-1 mice resulted in spontaneous pulmonary inflammation with features of type 2 immune responses and airway remodeling like those seen in mice with global deletion of SHIP-1. Furthermore, when compared to wild-type control mice, Tek-Cre/SHIP-1 mice displayed a significant increase in the number of IL-5/IL-13 producing ILC2 cells in the lung at baseline and after stimulation by allergen Papain. These findings provide some hints that PI3K signaling may play a role in ILC2 cell development at baseline and in response to allergen stimulation. SHIP-1 is required for maintaining lung homeostasis potentially by restraining ILC2 cells and type 2 inflammation.

scholarly journals The plasminogen system and cell surfaces: evidence for plasminogen and urokinase receptors on the same cell type.

1986 ◽  
Vol 103 (6) ◽  
pp. 2411-2420 ◽  
Author(s):  
E F Plow ◽  
D E Freaney ◽  
J Plescia ◽  
L A Miles
Keyword(s):  
Cell Line ◽  
Plasminogen Activator ◽  
Cell Lines ◽  
Specific Binding ◽  
High Capacity ◽  
Fetal Lung ◽  
Fibroblast Cell ◽  
Cell Types ◽  
Cell Surfaces ◽  
Catalytically Active

The capacity of cells to interact with the plasminogen activator, urokinase, and the zymogen, plasminogen, was assessed using the promyeloid leukemic U937 cell line and the diploid fetal lung GM1380 fibroblast cell line. Urokinase bound to both cell lines in a time-dependent, specific, and saturable manner (Kd = 0.8-2.0 nM). An active catalytic site was not required for urokinase binding to the cells, and 55,000-mol-wt urokinase was selectively recognized. Plasminogen also bound to the two cell lines in a specific and saturable manner. This interaction occurred with a Kd of 0.8-0.9 microM and was of very high capacity (1.6-3.1 X 10(7) molecules bound/cell). The interaction of plasminogen with both cell types was partially sensitive to trypsinization of the cells and required an unoccupied high affinity lysine-binding site in the ligand. When plasminogen was added to the GM1380 cells, a line with high intrinsic plasminogen activator activity, the bound ligand was comprised of both plasminogen and plasmin. Urokinase, in catalytically active or inactive form, enhanced plasminogen binding to the two cell lines by 1.4-3.3-fold. Plasmin was the predominant form of the bound ligand when active urokinase was added, and preformed plasmin can also bind directly to the cells. Plasmin on the cell surface was also protected from its primary inhibitor, alpha 2-antiplasmin. These results indicate that the two cell lines possess specific binding sites for plasminogen and urokinase, and a family of widely distributed cellular receptors for these components may be considered. Endogenous or exogenous plasminogen activators can generate plasmin on cell surfaces, and such activation may provide a mechanism for arming cell surfaces with the broad proteolytic activity of this enzyme.

High concentrations of oxygen modulate in vitro Con A responses of rat lymphoid cells. Effect of 2-mercaptoethanol

1985 ◽  
Vol 11 (1) ◽  
pp. 51-55 ◽  
Author(s):  
Laurence Kraus ◽  
Philippe Lacombe ◽  
Michel Fay ◽  
Jean-Jacques Pocidalo
Keyword(s):  
Lymphoid Cells ◽  
Con A ◽  
High Concentrations
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