Related Experiment Video
Updated: Aug 30, 2026

Multiomics Analysis of TMEM200A as a Pan-Cancer Biomarker
Published on: September 15, 2023
CD200 is a novel p53-target gene involved in apoptosis-associated immune tolerance
Michael D Rosenblum1, Edit Olasz, Jeffery E Woodliff
1Department of Pediatrics, Medical College of Wisconsin, Milwaukee 53226, USA.
Abstract:
During apoptotic cell death, biochemical processes modify self-proteins and create potential autoantigens. To maintain self-tolerance in the face of natural cell turnover, the immune system must prevent or control responses to apoptosis-associated autoantigens or risk autoimmunity. The molecular mechanisms governing this process remain largely unknown. Here, we show that expression of the immunoregulatory protein CD200 increases as murine dendritic cells (DCs) undergo apoptosis. We define CD200 as a p53-target gene and identify both p53- and caspase-dependent pathways that control CD200 expression during apoptosis. CD200 expression on apoptotic DCs diminishes proinflammatory cytokine production in response to self-antigens in vitro and is required for UVB-mediated tolerance to haptenated self-proteins in vivo. Up-regulation of CD200 may represent a novel mechanism, whereby immune reactivity to apoptosis-associated self-antigens is suppressed under steady state conditions.
Insights
The immune system must control responses to self-antigens released during cell death to prevent autoimmunity. This study reveals that CD200 protein expression increases on dying dendritic cells (DCs), suppressing immune responses to self-antigens.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- Apoptosis (programmed cell death) generates self-antigens that can trigger autoimmune responses.
- Mechanisms controlling immune tolerance to self-antigens during cell turnover are not fully understood.
- Dendritic cells (DCs) play a critical role in initiating immune responses and maintaining self-tolerance.
Purpose of the Study:
- To investigate the molecular mechanisms regulating immune responses to apoptosis-associated self-antigens.
- To identify novel immunoregulatory molecules involved in maintaining self-tolerance during cell death.
- To elucidate the role of CD200 in the immune response to apoptotic cells.
Main Methods:
- Analysis of CD200 protein expression in murine dendritic cells (DCs) undergoing apoptosis.
- Identification of regulatory pathways (p53, caspase-dependent) controlling CD200 expression during apoptosis.
- In vitro assays measuring proinflammatory cytokine production in response to self-antigens.
- In vivo studies assessing UVB-mediated tolerance to haptenated self-proteins.
Main Results:
- CD200 expression is upregulated on murine DCs during apoptosis.
- CD200 is identified as a p53-target gene, with its expression regulated by p53- and caspase-dependent pathways.
- CD200 on apoptotic DCs suppresses proinflammatory cytokine production in vitro.
- CD200 is essential for UVB-induced tolerance to haptenated self-proteins in vivo.
Conclusions:
- Upregulation of CD200 on apoptotic DCs is a novel mechanism for suppressing immune reactivity to self-antigens.
- This CD200-mediated suppression is crucial for maintaining self-tolerance under steady-state conditions.
- Understanding these pathways may offer therapeutic targets for autoimmune diseases.
More Related Videos
Related Concept Videos
The Intrinsic Apoptotic Pathway
The Extrinsic Apoptotic Pathway
Abnormal Proliferation
Cancer-Critical Genes II: Tumor Suppressor Genes
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes II: Tumor Suppressor Genes
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cellular Injury V: Apoptosis and Autophagy

