You will be shown an abstract from a biomedical research paper. Given this abstract, your task is to extract all unique entities of the following types: ["RNA", "CellLine", "Protein", "DNA", "CellType"].

Please return the output as a JSON object of the format: {"DNA" : ["TAL1", ...], "RNA": ["mRNAs", ...], "CellLine": ["T cells", ...], "CellType": ["monocytes", ...], "Protein": ["IL-2", ...]}. The keys should be entity types and values should be lists of extracted entities belonging to the corresponding type. If you cannot find entities belonging to a specific type, the value should be [].

Only output the JSON object and do not include any additional text.

Abstract:

Human T cell activation through the activation-inducer molecule / CD69 enhances the activity of transcription factor AP-1. The induction of the AP-1 transcription factor has been ascribed to the early events leading to T cell differentiation and activation. We have studied the regulation of AP-1 activity in human peripheral blood T lymphocytes stimulated through the activation inducer molecule (AIM) / CD69 activation pathway. Phorbol esters are required to induce AIM / CD69 cell-surface expression as well as for triggering the proliferation of T cells in conjunction with anti-AIM mAb. Mobility shift assays showed that addition of anti-AIM mAb to PMA-treated T lymphocytes markedly enhanced the binding activity of AP-1 to its cognate sequence, the phorbol ester response element. In contrast, anti-AIM mAb did not induce any change in the binding activity of NF-kappa B, a transcription factor whose activity is also regulated by protein kinase C. The increase in AP-1-binding activity was accompanied by the marked stimulation of the transcription of c-fos but not that of c-jun. Blockade of the DNA-binding complexes with an anti-Fos mAb demonstrated a direct participation of c-Fos in the AP-1 complexes induced by anti-AIM mAb. Most of the AP-1 activity could be eliminated when the anti-AIM mAb was added to the culture medium in the presence of cycloheximide, suggesting that de novo protein synthesis is crucial for the induction of AP-1-binding activity. These data provide the evidence that activation of human peripheral blood T cells through the AIM activation pathway regulate the activity of AP-1. Therefore, this pathway appears as a crucial step in the initiation of early T cell activation events.
{"CellLine": [], "CellType": ["human peripheral blood T lymphocytes", "PMA - treated T lymphocytes", "human peripheral blood T cells", "T cells", "T lymphocytes"], "DNA": ["phorbol ester response element"], "Protein": ["AIM / CD69", "AP - 1 transcription factor", "the AP - 1 transcription factor", "AP - 1", "protein kinase C", "c - Fos", "activation - inducer molecule / CD69", "c - fos", "CD69", "anti - Fos mAb", "transcription factor AP - 1", "NF - kappa B", "AP - 1 complexes", "DNA - binding complexes", "the AP - 1 complexes", "PMA", "c - jun", "anti - AIM mAb", "the anti - AIM mAb", "transcription factor"], "RNA": []}