scholarly journals Induction of neonatal tolerance to H-2k in B6 mice does not allow the emergence of T cells specific for H-2k plus vaccinia virus.

1982 ◽  
Vol 156 (3) ◽  
pp. 810-821 ◽  
Author(s):  
D H Schwartz ◽  
P C Doherty
Keyword(s):  
T Cells ◽  
T Cell ◽  
Vaccinia Virus ◽  
Somatic Mutation ◽  
T Lymphocyte ◽  
Cytotoxic T Lymphocyte ◽  
Spleen Cells ◽  
Cell Ontogeny ◽  
Stimulation Of ◽  
Tolerized Mouse

Thymocytes and spleen cells from C57BL/6 mice (H-2b) neonatally tolerized to H-2k alloantigens do not generate an anti-vaccinia response restricted to H-2Kk when adoptively transferred to appropriate irradiated hosts. This is in sharp contrast to the case for negatively selected C57BL/6 spleen cells acutely depleted of alloreactivity. No evidence for suppression was found in cell mixture experiments. We have shown elsewhere that our neonatally tolerized animals have a centrally induced delection-type tolerance in the absence of obvious suppression.2 We now suggest that in the neonatally tolerized mouse, chronic, central delection of anti-H-2k clones during early T cell ontogeny eliminates the major source of cells able to give rise, via somatic mutation and expansion, to anti-H-2Kk + vaccinia specific cytotoxic T lymphocyte precursors (CTL-P) in the adult. A similar mechanism may operate in the (k + b) leads to b chimera; however, the presence of H-2kxb accessory and presenting cells may permit the eventual generation (via cross-stimulation) of an H-2k-restricted vaccinia-specific repertoire. This would account for our observation of such "aberrant recognition" CTL-P emerging in the spleens of older (k x b) leads to b chimeras.

scholarly journals Indirect allorecognition of platelets by T helper cells during platelet transfusions correlates with anti-major histocompatibility complex antibody and cytotoxic T lymphocyte formation [published erratum appears in Blood 1995 Dec 15;86(12):4710]

Blood ◽  
1995 ◽  
Vol 86 (2) ◽  
pp. 805-812 ◽  
Author(s):  
JW Semple ◽  
ER Speck ◽  
YP Milev ◽  
V Blanchette ◽  
J Freedman
Keyword(s):  
T Cells ◽  
Major Histocompatibility Complex ◽  
T Cell ◽  
Mhc Class I ◽  
T Lymphocyte ◽  
Nk Cell ◽  
Cytotoxic T Lymphocyte ◽  
Spleen Cells ◽  
Histocompatibility Complex ◽  
Platelet Transfusions

To study the cellular immunology of platelet-induced alloimmunization, a murine transfusion model was developed. BALB/c (H-2d) recipient mice were transfused weekly with 2 x 10(8) platelets or 10(3) leukocytes from C57BL/6 (H-2b) donor mice. Recipient antidonor major histocompatibility complex (MHC) class I alloantibodies could be detected in flow cytometric assays by the fifth platelet transfusion. In contrast, when leukocytes only were transfused, alloantibodies were not detected. In vitro assays demonstrated that murine H-2b platelets were positive for MHC class I expression but lacked MHC class II molecules on their membranes and were unable to stimulate proliferation or cytokine production when incubated with naive H-2d spleen cells. In vivo, however, platelet transfusions induced two distinct patterns of cell-mediated reactivity. First, during the initial transfusions and before alloantibody formation, there was induction of T-cell anergy, characterized by the inability of recipient T cells to respond to Concanavalin A (ConA) or to proliferate in an antidonor mixed lymphocyte reaction (MLR), together with suppressed natural killer (NK) cell activity. This unresponsiveness was associated with a transient increase in nitric oxide (NO)-dependent cytotoxicity and interleukin-1 (IL-1) production. Second, once alloantibodies developed, significantly increased antidonor CD8+ cytotoxic T lymphocyte (CTL) and NK cell responses were observed. At this time, when recipient spleen cells were depleted of CD8+ T cells and incubated with only donor platelets in 7- day antigen-presenting cell (APC) assays, enhanced proliferation and IL- 2 production occurred. These cellular responses were not seen when 10(3) allogeneic leukocytes were transfused. Thus, the results suggest that leukoreduced platelet transfusions induce antidonor MHC antibodies and CD8+ CTL responses in recipient mice. At the same time, the transfusions induced recipient CD4+ T-cell activation when incubated with donor platelets in the presence of syngeneic APCs, an indirect recognition pathway that correlates with the time of alloantibody production.

Stimulation of Peripheral Blood T Cells by an Activated T-Cell Line: a Novel Human Autologous T-T Lymphocyte Reaction

1991 ◽  
Vol 34 (6) ◽  
pp. 713-719 ◽  
Author(s):  
R. DITZIAN-KADANOFF ◽  
L. PARKS ◽  
B. EVAVOLD ◽  
J. QUINTANS ◽  
T. J. SWARTZ
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Line ◽  
T Lymphocyte ◽  
Peripheral Blood ◽  
Activated T Cell ◽  
Stimulation Of

scholarly journals Ligation of Cytotoxic T Lymphocyte Antigen-4 to T Cell Receptor Inhibits T Cell Activation and Directs Differentiation into Foxp3+Regulatory T Cells

2012 ◽  
Vol 287 (14) ◽  
pp. 11098-11107 ◽  
Author(s):  
Jozsef Karman ◽  
Ji-Lei Jiang ◽  
Nathan Gumlaw ◽  
Hongmei Zhao ◽  
Juanita Campos-Rivera ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Regulatory T Cells ◽  
T Cell Receptor ◽  
T Cell Activation ◽  
T Lymphocyte ◽  
Cell Activation ◽  
Cytotoxic T Lymphocyte ◽  
Cell Receptor ◽  
Lymphocyte Antigen

scholarly journals Selective suppression of the major idiotypic component of an antihapten response by soluble T cell-derived factors with idiotypic or anti-idiotypic receptors.

1980 ◽  
Vol 151 (5) ◽  
pp. 1213-1231 ◽  
Author(s):  
Y Hirai ◽  
A Nisonoff
Keyword(s):  
Molecular Weight ◽  
T Cells ◽  
T Cell ◽  
Gel Filtration ◽  
Humoral Response ◽  
Spleen Cells ◽  
Suppressor T Cells ◽  
Soluble Factors ◽  
Selective Suppression ◽  
Stimulation Of

Evidence is presented for the selective suppression of the major idiotypic component of the humoral response to the phenylarsonate hapten by soluble factors derived from T cells (TsF). The existence of TsF with anti-idiotypic receptors was also demonstrated. It was found that TsF with idiotypic and anti-idiotypic receptors coexist in cultures of spleen cells prepared from idiotypically suppressed, hyperimmunized mice. By gel filtration the molecular weight of each factor was found to be 50,000-100,000. Each is sensitive to trypsin and is bound to a column containing anti-H-2a antibodies. Evidence is discussed which suggests the possibility of mutual stimulation of suppressor T cells with idiotypic and anti-idiotypic receptors.

scholarly journals Cytotoxic T Lymphocyte–associated Antigen 4 (CTLA-4) Can Regulate Dendritic Cell–induced Activation and Cytotoxicity of CD8+ T Cells Independently of CD4+T Cell Help

1999 ◽  
Vol 189 (7) ◽  
pp. 1157-1162 ◽  
Author(s):  
Kathy D. McCoy ◽  
Ian F. Hermans ◽  
J. Henry Fraser ◽  
Graham Le Gros ◽  
Franca Ronchese
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Lymphocyte ◽  
Cd8 T Cells ◽  
Cytotoxic T Lymphocyte ◽  
Cd4 T Cell ◽  
Cd4 T Cell Help ◽  
T Cell Help

The mechanisms that regulate the strength and duration of CD8+ cytotoxic T cell activity determine the effectiveness of an antitumor immune response. To better understand the antitumor effects of anti-cytotoxic T lymphocyte–associated antigen 4 (CTLA-4) antibody treatment, we analyzed the effect of CTLA-4 signaling on CD8+ T cells in vitro and in vivo. In vitro, cross-linking of CTLA-4 on purified CD8+ T cells caused decreased proliferative responses to anti-CD3 stimulation and rapid loss of activation marker expression. In vivo, blockade of CTLA-4 by neutralizing anti–CTLA-4 mAb greatly enhanced the accumulation, activation, and cytotoxic activity of CD8+ T cells induced by immunization with Ag on dendritic cells (DC). This enhanced response did not require the expression of MHC class II molecules on DC or the presence of CD4+ T cells. These results demonstrate that CTLA-4 blockade is able to directly enhance the proliferation and activation of specific CD8+ T cells, indicating its potential for tumor immunotherapy even in situations in which CD4+ T cell help is limited or absent.

scholarly journals Cytotoxic T Lymphocyte Antigen Costimulation Influences T-Cell Activation in Response to Cryptococcus neoformans

2001 ◽  
Vol 69 (3) ◽  
pp. 1508-1514 ◽  
Author(s):  
Donatella Pietrella ◽  
Stefano Perito ◽  
Francesco Bistoni ◽  
Anna Vecchiarelli
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cryptococcus Neoformans ◽  
T Cell Activation ◽  
T Lymphocyte ◽  
Mononuclear Cells ◽  
Cytotoxic T Lymphocyte ◽  
Interleukin 2 ◽  
T Cell Response ◽  
Lymphocyte Antigen

ABSTRACT The kinetics of cytotoxic T lymphocyte antigen 4 (CTLA-4) expression on T cells responding to Cryptococcus neoformansand its role in regulating the T-cell response were examined. Using peripheral blood mononuclear cells stimulated with encapsulated or acapsular C. neoformans we showed that (i) the encapsulated strain augmented CTLA-4 expression on the T-cell surface while the acapsular strain was a weaker modulator, (ii) CTLA-4 molecules were rapidly up-regulated after the addition of encapsulated C. neoformans, (iii) CTLA-4 was up-regulated predominantly in CD4+ T cells responding to C. neoformans, and (iv) blockage of CTLA-4 with (Fab′)2 of monoclonal antibody to CTLA-4 induced T-cell proliferation that paralleled the enhancement of interleukin-2 and gamma interferon production. These results suggest that capsular material, the major virulence factor of C. neoformans, promotes synthesis and expression of CTLA-4 molecules predominantly in CD4+ T cells. CTLA-4-mediated deactivation is due not to lack of costimulation but to specific recognition of CTLA-4 for B7 molecules. This appears to be a new mechanism by whichC. neoformans may elude the host immune response.

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