T Cell Activation Pathways: B7, LFA-3, and ICAM-1 Shape Unique T Cell Profiles

Wingren, Anette Gjörloff; Parra, Eduardo; Varga, Mikael; Kalland, Terje; Sjögren, Hans; Hedlund, Gunnar; Dohlsten, Mikael

doi:10.1615/critrevimmunol.v15.i3-4.30

Cited by 149 publications

(63 citation statements)

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“…4b) and DNA synthesis determined by [ 3 H]thymidine incorporation assay (data not shown). Failure to induce T cell proliferation by Tat alone is consistent with the ''two-signal'' model for T cell activation (28). Cyclin E-associated cdk activity of Tat-treated lymphocytes was induced, similar to that of proliferating lymphocytes treated with phytohemagglutinin plus human recombinant interleukin 2 (Fig.…”

Section: Activation Of Primary T Cells By Tat Protein Involvessupporting

confidence: 80%

Tat protein induces self-perpetuating permissivity for productive HIV-1 infection

Ueda

Shi

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

106

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We report that human immunodeficiency virus type 1 (HIV-1) has evolved a self-perpetuating mechanism to actively generate cells permissive for productive and cytopathic infection. Only activated T cells can be productively infected, which leads to their rapid depletion (2 ؋ 10 9 ͞day in an infected individual). Establishment of productive HIV-1 infection therefore requires continual activations from the large pool of quiescent T cells. Tat protein, which is secreted by infected cells, activated uninfected quiescent T cells in vitro and in vivo. These Tat-activated uninfected cells became highly permissive for productive HIV-1 infection. Activation of primary T cells by Tat protein involved integrin receptors and was associated with activation of mitogen-activated protein kinases, including ERK1 and JNK kinase. Accordingly, these primary T cells progressed from G 0 to the late G 1 phase of the cell cycle.

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Section: Activation Of Primary T Cells By Tat Protein Involvessupporting

confidence: 80%

Tat protein induces self-perpetuating permissivity for productive HIV-1 infection

Ueda

Shi

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

106

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“…Although there have been a number of studies on the role of accessory molecules in T-cell activation, [4][5][6][7][8][9][10] only a few studies have begun to address the role of the costimulatory molecules on enhancing the stimulation of effector/memory cells. [11][12][13][14][15] To this end, we have investigated the consequence of infected tumor target cells with fowlpox (FP) viruses containing various costimulatory molecules on enhancing the activity of the effector/memory CD8 þ cells in the lysis of those target cells.…”

mentioning

confidence: 99%

Amplification of the lytic potential of effector/memory CD8+ cells by vector-based enhancement of ICAM-1 (CD54) in target cells: implications for intratumoral vaccine therapy

et al. 2004

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We demonstrated that enhanced expression of the costimulatory molecules CD80, CD54 and CD48 (designated rF-TRICOM) on target cells, as delivered via a recombinant fowlpox vector, results in an increased state of stimulation of CD8 þ T cells, and consequent increased lysis of target cells. CTL studies in conjunction with antibody-blocking studies demonstrated that the enhanced effector activity of these CD8 þ T cells is mediated mainly through CD54. Intracellular staining of CD8 þ cells that interact with target cells infected with rF-TRICOM showed that they contain higher amounts of perforin and have a higher level of perforin message. Enhanced expression of costimulatory molecules (specifically CD54) on target cells using rF-TRICOM vectors also leads to the formation of stable conjugates/synapses between targets and T cells. The interaction of T cells with target cells that overexpress costimulatory molecules upon infection with rF-TRICOM leads to enhanced signaling through Lck, ZAP70, and STAT-1 in CD8 þ T cells and heightened lytic activity of CD8 þ cells through the formation of a greater number of immunological synapses. This, in turn, leads to enhanced signaling in T cells. Finally, studies were conducted in mice in which CEA is a self-antigen in an attempt to understand the potential clinical relevancy of intratumoral vaccine therapy. Mice were transplanted subcutaneously with CEA expressing tumors. Intratumoral (i.t.) vaccination was administered 8 days post tumor transplant. Mice vaccinated i.t. with rF-TRICOM demonstrated significantly reduced tumor growth and 40% of the mice had complete tumor regression. The antitumor effects were further improved by the addition of tumor antigen (CEA) in the vaccination by utilizing rF-CEA/TRICOM, with 80% of the mice experiencing complete tumor regression. These studies thus support the concept of intratumoral vaccination employing vectors expressing costimulatory molecules.

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“…In contrast, blocking the reaction between the intercellular adhesion molecule 1 (ICAM1) and lymphocyte function antigen 1 (LFA1) appeared to be associated with immunosuppression. Important contributors to T cell activation have been reviewed by Wingren et al (1995) and include the work of Ford and Larsen (2009). The work of Jenkins, Schwartz, and colleagues has shown antigen specific T cell unresponsiveness , Jenkins and Schwartz, 2009.…”

Section: Costimulation Blockade To Interrupt the Process Of T Cell Acmentioning

confidence: 99%

Immunological Considerations for Inducing Skin Graft Tolerance

Gordon¹

2011

Skin Grafts - Indications, Applications and Current Research

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T Cell Activation Pathways: B7, LFA-3, and ICAM-1 Shape Unique T Cell Profiles

Cited by 149 publications

References 0 publications

Tat protein induces self-perpetuating permissivity for productive HIV-1 infection

Tat protein induces self-perpetuating permissivity for productive HIV-1 infection

Amplification of the lytic potential of effector/memory CD8+ cells by vector-based enhancement of ICAM-1 (CD54) in target cells: implications for intratumoral vaccine therapy

Immunological Considerations for Inducing Skin Graft Tolerance

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