<b>Enhancement of CD3‐mediated thymocyte apoptosis by the cross‐linkage of heat‐stable antigen</b>

Hitsumoto, Yasuo; Song, D.‐S.; Okada, Masato; Hamada, Fumihiko; Saheki, Shûichi; Takeuchi, N.

doi:10.1046/j.1365-2567.1996.d01-741.x

Cited by 6 publications

(4 citation statements)

References 37 publications

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“…2). Our present findings differ from those of Hitsumoto et al (15) and Punt et al (3), who found that CD24 ligation only enhanced the CD3-mediated death of thymocytes. We assume that this could come from different approaches applied in our system for the detection of apoptotic cells.…”

Section: Discussioncontrasting

confidence: 99%

“…In fact, in human B cell lines, CD24 engagement by specific Abs induces apoptosis, which does not require B cell receptor signaling (16,17). In contrast, CD24 ligation in mouse thymocytes has been reported to enhance CD3-mediated apoptosis, but CD24 engagement alone did not cause thymocyte apoptosis (15).…”

mentioning

confidence: 97%

“…CD24 expressed on the activated T cells is also known as a signaling molecule, thus the possibility of homophilic interaction between CD24 molecules on T lymphocytes and APCs was suggested (14). In addition, CD24 appears to be involved in the apoptosis of B cells and thymocytes (3,(15)(16)(17). In fact, in human B cell lines, CD24 engagement by specific Abs induces apoptosis, which does not require B cell receptor signaling (16,17).…”

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confidence: 99%

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TCR-Independent and Caspase-Independent Apoptosis of Murine Thymocytes by CD24 Cross-Linking

Jung

Park

Kim

et al. 2004

The Journal of Immunology

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CD24, also referred to as the heat-stable Ag, is a T cell differentiation Ag that is highly expressed on both CD4−CD8− double negative and CD4+CD8+ double positive thymocytes. Here, we report that CD24 ligation by a new anti-CD24 Ab, mT-20, induced the apoptosis of both double negative and double positive thymocytes, as well as the Scid.adh thymic lymphoma cell line, in the absence of TCR/CD3 engagement. CD24-mediated apoptosis of mouse thymocytes and its signaling pathway appeared not to be associated with p53, CD95, TNFR, or caspases. Furthermore, we found that cell death was blocked by the addition of scavengers of reactive oxygen species or by Bcl-2 overexpression, implying the role of CD24 signaling in the mitochondrial regulation. In this study, we suggest that CD24 ligation induced the apoptosis of immature thymocytes independently of both caspase and TCR.

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confidence: 99%

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confidence: 97%

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confidence: 99%

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TCR-Independent and Caspase-Independent Apoptosis of Murine Thymocytes by CD24 Cross-Linking

Jung

Park

Kim

et al. 2004

The Journal of Immunology

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“…Blocking antibodies against CD24 led to non-CD8 + T cell-dependent death of the mice due to possible anaphylaxis when given with vaccine (data not shown). CD24 has also been shown to be involved in apoptosis in B cells and tumor cells as well as T cells indicating that had CD24-blocking antibody not been lethal in those conditions it may have had side effects counterproductive to tumor elimination (41–44). …”

Section: Discussionmentioning

confidence: 99%

Apoptosis-Regulated Low-Avidity Cancer-Specific CD8+ T Cells Can Be Rescued to Eliminate HER2/neu–Expressing Tumors by Costimulatory Agonists in Tolerized Mice

Black

Armstrong

Jaffee

2014

Cancer Immunology Research

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A major barrier of vaccines as cancer treatment is their failure to activate and maintain a complete cancer-specific CD8+ effector T cell repertoire. Low avidity T cells are more likely to escape clonal deletion in the thymus when compared to higher avidity T cells, and therefore comprise the major population of effector T cells available for activation in cancer patients. However, low avidity T cells fail to traffic into the tumor microenvironment and function in eradicating tumor under optimal vaccination conditions as opposed to higher avidity T cells that escape clonal deletion and function in tumor-killing. We utilized high and low avidity TCR transgenic CD8+ T cells specific for the immunodominant epitope HER-2/neu (RNEU420-429) to identify signaling pathways responsible for the inferior activity of the low avidity T cells. Adoptive transfer of these cells into tumor-bearing vaccinated mice identified members of apoptosis pathways that are upregulated in low avidity T cells. The increased expression of pro-apoptotic proteins by low avidity T cells promoted their own cell death and also that of other tumor-specific CD8+ T cells within their local environment. Importantly, we show that this pro-apoptotic effect can be overcome using a strong costimulatory signal that prevents activation-induced cell death and enables low avidity T cells to traffic into the tumor and assist in tumor clearance. These findings identify new therapeutic opportunities for activating the most potent anticancer T cell responses.

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Kinetics and differential expression of heat-stable antigen and GL7 in the normal and Toxoplasma gondii -infected murine brain

Deckert-Schlüter

Buck²,

Schlüter

1999

Acta Neuropathologica

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The co-expression of various cell surface molecules by cells of the nervous system and the immune system is a remarkable feature. To identify novel molecules that are shared between cells of the neural and hematopoietic lineage, the expression and regulation of heat-stable antigen (HSA, CD24, nectadrin) and GL7, two hematolymphoid differentiation antigens that are involved in antigen presentation, cell adhesion, signal transduction and activation, was studied in the adult normal and Toxoplasma gondii-infected murine brain by immunohistochemistry and flow cytometry of isolated cerebral leukocytes. In the normal brain ependymal cells, plexus macrophages and a fraction of blood vessel endothelial cells were HSA positive (+), whereas the choroid plexus epithelium was GL7+. This basal expression of HSA and GL7 was not further modified on these cell populations in Toxoplasma encephalitis (TE). In acute and chronic TE, HSA and GL7 were strongly induced on resident brain cells, and activated astrocytes were the predominant HSA+ and GL7+ cell type. FACS analysis additionally identified a minor fraction of HSA+ microglia in the normal brain with a small, but significant increase in TE. The differential expression pattern of HSA and GL7 on distinct resident cell populations in various anatomic compartments of the normal adult brain and their up-regulation in TE may indicate that their intracerebral role is diverse and may include both immunological as well as non-immunological functions.

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Enhancement of CD3‐mediated thymocyte apoptosis by the cross‐linkage of heat‐stable antigen

Cited by 6 publications

References 37 publications

TCR-Independent and Caspase-Independent Apoptosis of Murine Thymocytes by CD24 Cross-Linking

TCR-Independent and Caspase-Independent Apoptosis of Murine Thymocytes by CD24 Cross-Linking

Apoptosis-Regulated Low-Avidity Cancer-Specific CD8+ T Cells Can Be Rescued to Eliminate HER2/neu–Expressing Tumors by Costimulatory Agonists in Tolerized Mice

Kinetics and differential expression of heat-stable antigen and GL7 in the normal and Toxoplasma gondii -infected murine brain

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