| DB ID | MyCo_5640 |
| Title | Protective Activity of Programmed Cell Death Protein 1 Blockade and Synergy With Caspofungin in a Murine Invasive Pulmonary Aspergillosis Model |
| Year | 2020 |
| PMID | 32432714 |
| Fungal Diseases involved | Invasive pulmonary aspergillosis |
| Associated Medical Condition | None |
| Genus | Aspergillus |
| Species | fumigatus |
| Organism | Aspergillus fumigatus |
| Ethical Statement | All experiments were approved by the MD Anderson Cancer Center Institutional Animal Care and Use Committee (protocol 00001734-RN00). |
| Site of Infection | None |
| Opportunistic invasive | Invasive/Opportunistic |
| Sample type | Biopsy |
| Sample source | Homogenized Lungs tissue |
| Host Group | Animal |
| Host Common name | Mice |
| Host Scientific name | Mus musculus |
| Biomarker Name | PD-1 |
| Biomarker Full Name | Pro-grammed cell death protein 1 |
| Biomarker Type | Diagnostic |
| Biomolecule | Protein |
| Geographical Location | USA |
| Cohort | Female 8–12-week-old BALB/cAnNCrl inbred mice (Charles River Laboratories) with a weight of 20–25 g were immuno- suppressed with cyclophosphamide (Sigma-Aldrich, 150 mg/ kg body weight on days −4 and −1, 100 mg/kg on day +3) and cortisone acetate (Sigma-Aldrich, 300 mg/kg on day −1). Mice were infected intranasally with 5 × 104 A. fumigatus Af-293 conidia. |
| Cohort No. | None |
| Age Group | None |
| P Value | None |
| Sensitivity | None |
| Specificity | None |
| Positive Predictive Value | None |
| MIC | None |
| Fold Change | None |
| Pathway | None |
| Disease Introduction Mechanism | Opportunistic mold infections including invasive pulmonary aspergillosis (IPA) remain a major source of disease and death in immunocompromised patients. Because current antifungal pharmacotherapy is suboptimal in the setting of impaired host immunity, there is an unmet need for adjunct immune en- hancement strategies to potentiate the efficacy of antifungals. Although cellular immunotherapies such as adoptive T-cell transfer or chimeric antigen receptor T cells or natural killer cells may have game-changing potential, their translatability to the bedside is complicated by logistical, regulatory, and eco- nomic hurdles. Immune checkpoint inhibitor (CPI) therapy, a widely available immunotherapeutic strategy that already has proven value in modern oncology, could overcome these obs- tacles and is gaining interest for applications in the field of infectious diseases. |
| Technique | PCR |
| Analysis Method | qRT-PCR |
| ELISA kits | None |
| Assay Data | None |
| Validation Techniques used | qRT-PCR |
| Up Regulation Down Regulation | Increase |
| Sequence Data | None |
| External Link | None |
