scholarly journals Definition of conditions that enable antigen-specific activation of the majority of isolated trinitrophenol-binding B cells.

1982 ◽  
Vol 156 (6) ◽  
pp. 1635-1649 ◽  
Author(s):  
J C Cambier ◽  
J G Monroe ◽  
M J Neale
Keyword(s):  
Cell Cycle ◽  
T Cell ◽  
Interleukin 1 ◽  
Isolated Cells ◽  
Cellular Events ◽  
Accessory Cells ◽  
B Cell Growth Factor ◽  
Human Gamma Globulin ◽  
Definition Of ◽  
T Cell Help

In an effort to further elucidate the early cellular events in generation of antibody responses, we have determined the requirements for antigen-specific initiation of the G0 to G1 transition by isolated trinitrophenol (TNP) -binding B lymphocytes. TNP-binding cells were isolated from normal B6D2F1 splenocyte populations using hapten affinity fractionation on disulfide-bonded TNP-gelatin-coated plates. Populations prepared in this way are greater than or equal to 96% immunoglobulin positive and 70-95% antigen binding. Isolated cells were cultured for 48 h in the presence of a variety of TNP conjugates including TNP-Brucella abortus (Ba), TNP-Ficoll, TNP-sheep erythrocytes (SRBC), TNP-human gamma globulin (HGG), or TNP-ovalbumin (OVA) before being harvested and subjected to acridine orange cell cycle analysis. As many as 80% of cells were in cycle by 48 h in response to TNP-Ba, a thymus-independent (TI1 antigen. A smaller proportion (congruent to 40%) were in cycle in response to TNP-Ficoll, a TI2 antigen. Significant activation was not detected in cultures challenged with the thymus-dependent immunogens TNP-SRBC, TNP-HGG, and TNP-OVA. Addition of interleukin 1 (IL-1), IL-2, B cell growth factor, and/or T cell-replacing factor to cultures did not facilitate responses to these immunogens, suggesting a requirement for antigen-specific T cell help for entry into cell cycle induced by thymus dependent antigens. Activation by TNP-Ba was antigen specific and independent of accessory cells, occurring with equal efficiency in bulk and single-cell cultures. Activation by TNP-Ba was inhibitable by anti-Fab and anti-mu antibodies, but not by anti-delta antibodies. Results indicate that activation of TNP-binding cells to enter cell cycle by TNP-Ba is independent of accessory cells and requires interaction of antigen with cell surface IgM. Exposure to thymus-dependent TNP-immunogens plus nonspecific helper factors is insufficient to cause entry of TNP-binding cells into cycle.

scholarly journals T cell help controls the speed of the cell cycle in germinal center B cells

Science ◽  
2015 ◽  
Vol 349 (6248) ◽  
pp. 643-646 ◽  
Author(s):  
A. D. Gitlin ◽  
C. T. Mayer ◽  
T. Y. Oliveira ◽  
Z. Shulman ◽  
M. J. K. Jones ◽  
...  
Keyword(s):  
Cell Cycle ◽  
T Cell ◽  
B Cells ◽  
Germinal Center ◽  
T Cell Help ◽  
Germinal Center B Cells

scholarly journals Definition of T cell idiotypes using anti-idiotypic antisera produced by immunization with T cell clones.

1982 ◽  
Vol 155 (4) ◽  
pp. 1100-1107 ◽  
Author(s):  
A J Infante ◽  
P D Infante ◽  
S Gillis ◽  
C G Fathman
Keyword(s):  
T Cell ◽  
Cell Clone ◽  
Interleukin 2 ◽  
T Cell Proliferation ◽  
T Cell Clones ◽  
Cell Clones ◽  
Accessory Cells ◽  
T Cell Clone ◽  
Definition Of ◽  
Alloreactive T Cell

Alloreactive T cell clones with distinct specificities were used to raise anti-idiotypic antisera via an F1 anti-(parent anti-F1) protocol. Antisera were raised that could stimulate the proliferation of the appropriate T cell clone, but not other clones. The active fraction of the antisera for T cell proliferation was immunoglobulin. In addition to proliferation, an anti-idiotypic antiserum could induce the appropriate T cell clone to secrete substantial amounts of interleukin 2 (IL-2). Production of IL-2 appeared independent of the involvement of accessory cells. These accessory cells may be unnecessary for IL-2 production in our assay, or their effect may be produced by anti-idiotype. Thus, anti-idiotype may provide two or more specific T cell signals.

scholarly journals MicroRNA-155 is essential for the optimal proliferation and survival of plasmablast B cells

2019 ◽  
Vol 2 (3) ◽  
pp. e201800244 ◽  
Author(s):  
Giuseppina Arbore ◽  
Tom Henley ◽  
Laura Biggins ◽  
Simon Andrews ◽  
Elena Vigorito ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Comparative Analysis ◽  
T Cell ◽  
B Cells ◽  
Antibody Response ◽  
Antibody Production ◽  
Metabolic Process ◽  
Cellular Processes ◽  
T Cell Help

A fast antibody response can be critical to contain rapidly dividing pathogens. This can be achieved by the expansion of antigen-specific B cells in response to T-cell help followed by differentiation into plasmablasts. MicroRNA-155 (miR-155) is required for optimal T-cell–dependent extrafollicular responses via regulation of PU.1, although the cellular processes underlying this defect are largely unknown. Here, we show that miR-155 regulates the early expansion of B-blasts and later on the survival and proliferation of plasmablasts in a B-cell–intrinsic manner, by tracking antigen-specific B cells in vivo since the onset of antigen stimulation. In agreement, comparative analysis of the transcriptome of miR-155–sufficient and miR-155–deficient plasmablasts at the peak of the response showed that the main processes regulated by miR-155 were DNA metabolic process, DNA replication, and cell cycle. Thus, miR-155 controls the extent of the extrafollicular response by regulating the survival and proliferation of B-blasts, plasmablasts and, consequently, antibody production.

scholarly journals Helper signals in the plaque-forming cell response to protein-bound haptens.

1983 ◽  
Vol 158 (2) ◽  
pp. 317-333 ◽  
Author(s):  
N W Roehm ◽  
P Marrack ◽  
J W Kappler
Keyword(s):  
T Cell ◽  
B Cell ◽  
Cell Line ◽  
Interleukin 1 ◽  
Interleukin 2 ◽  
Tumor Cell Line ◽  
Con A ◽  
B Cell Growth Factor ◽  
Nonspecific Factors ◽  
Culture Supernatants

We have demonstrated the ability of a series of murine T cell hybridomas to deliver an antigen-specific, B cell I-region-restricted helper signal in the generation of specific PFC responses to protein-bound haptens. With some hybridomas the elicitation of optimal PFC responses required the addition of nonspecific factors provided by culture supernatants of concanavalin A-stimulated (Con A SN) spleen cells. Using hapten-primed B cells depleted of both T cells and macrophages (Mphi) we have now demonstrated a requirement for three nonspecific factor preparations to substitute for spleen Con A SN in the elicitation of optimal PFC responses. The first preparation was the interleukin 1 containing culture supernatant of the Mphi tumor cell line P388D1, the second the interleukin 2 (IL-2) and B cell growth factor containing Con A SN of the T cell hybridoma FS6-14.13, and the third, the gamma interferon containing Con A SN of the T cell hybridoma FS7-20.6.18. The P388D1 and FS6-14.13 factor preparations were most effective when added at the initiation of culture, while the FS7-20.6.18 factor preparation was most effective when added at 24 h of culture. The activity of FS6-14.13 Con A SN was depleted by incubation with the IL-2-dependent T cell line HT-2. The activity of FS7-20.6.18 Con A SN was abrogated by incubation at pH 2. The results suggest that the generation of PFC responses to protein-bound haptens require at least three nonspecific factors in addition to an antigen/Ia specific helper signal.

scholarly journals Modulation of in vitro eosinophil progenitors by hydrocortisone: role of accessory cells and interleukins

Blood ◽  
1985 ◽  
Vol 66 (5) ◽  
pp. 1072-1079
Author(s):  
FT Slovick ◽  
CN Abboud ◽  
JK Brennan ◽  
MA Lichtman
Keyword(s):  
T Cell ◽  
Cell Line ◽  
Conditioned Medium ◽  
Mononuclear Cells ◽  
Interleukin 1 ◽  
Interleukin 2 ◽  
Accessory Cell ◽  
Direct Function ◽  
Human Eosinophil ◽  
Accessory Cells

The growth of human eosinophil progenitors (CFU-Eo) and the modulation of growth by hydrocortisone were studied as functions of the presence of lymphocytes and monocytes in marrow cells under study; and the source of colony-stimulating factors, specifically, media conditioned by macrophage-like cell line, GCT; phytohemagglutinin-stimulated mononuclear cells (PHA-LCM); or the T cell line, MO. CFU-Eo growth was greatest in marrow containing accessory cells as compared to marrow depleted of accessory cells; and in marrow treated with phytohemagglutinin-stimulated leukocyte conditioned media (PHA-LCM) or MO (T cell line)-conditioned medium (MO-CM) as compared with GCT cell- conditioned medium (GCT-CM). Hydrocortisone reproducibly inhibited eosinophil progenitor growth in unfractionated marrow stimulated by GCT- CM. This effect was abrogated by admixing irradiated mononuclear cells or T lymphocytes with the target marrow or by adding interleukin 1 or interleukin 2 (IL-1, IL-2). Inhibition by hydrocortisone did not occur when monocyte and T lymphocyte depleted marrow was studied. Unlike GCT- CM, MO-CM and PHA-LCM stimulated equal proportions of eosinophil progenitors in nondepleted and accessory cell-depleted marrow and demonstrated less hydrocortisone inhibition. However, both GCT-CM and PHA-LCM produced in the presence of hydrocortisone stimulated significantly fewer CFU-Eos in both unfractionated and accessory cell- depleted marrow target populations. These results indicate that the growth of CFU-Eo and inhibition of growth by hydrocortisone is a direct function of a monocyte-T cell interaction and probably is mediated through effects on the production/release of eosinophil colony stimulating factor (Eo-CSF).

scholarly journals Modulation of in vitro eosinophil progenitors by hydrocortisone: role of accessory cells and interleukins

Blood ◽  
1985 ◽  
Vol 66 (5) ◽  
pp. 1072-1079 ◽  
Author(s):  
FT Slovick ◽  
CN Abboud ◽  
JK Brennan ◽  
MA Lichtman
Keyword(s):  
T Cell ◽  
Cell Line ◽  
Conditioned Medium ◽  
Mononuclear Cells ◽  
Interleukin 1 ◽  
Interleukin 2 ◽  
Accessory Cell ◽  
Direct Function ◽  
Human Eosinophil ◽  
Accessory Cells

Abstract The growth of human eosinophil progenitors (CFU-Eo) and the modulation of growth by hydrocortisone were studied as functions of the presence of lymphocytes and monocytes in marrow cells under study; and the source of colony-stimulating factors, specifically, media conditioned by macrophage-like cell line, GCT; phytohemagglutinin-stimulated mononuclear cells (PHA-LCM); or the T cell line, MO. CFU-Eo growth was greatest in marrow containing accessory cells as compared to marrow depleted of accessory cells; and in marrow treated with phytohemagglutinin-stimulated leukocyte conditioned media (PHA-LCM) or MO (T cell line)-conditioned medium (MO-CM) as compared with GCT cell- conditioned medium (GCT-CM). Hydrocortisone reproducibly inhibited eosinophil progenitor growth in unfractionated marrow stimulated by GCT- CM. This effect was abrogated by admixing irradiated mononuclear cells or T lymphocytes with the target marrow or by adding interleukin 1 or interleukin 2 (IL-1, IL-2). Inhibition by hydrocortisone did not occur when monocyte and T lymphocyte depleted marrow was studied. Unlike GCT- CM, MO-CM and PHA-LCM stimulated equal proportions of eosinophil progenitors in nondepleted and accessory cell-depleted marrow and demonstrated less hydrocortisone inhibition. However, both GCT-CM and PHA-LCM produced in the presence of hydrocortisone stimulated significantly fewer CFU-Eos in both unfractionated and accessory cell- depleted marrow target populations. These results indicate that the growth of CFU-Eo and inhibition of growth by hydrocortisone is a direct function of a monocyte-T cell interaction and probably is mediated through effects on the production/release of eosinophil colony stimulating factor (Eo-CSF).

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