RESUMEN
BACKGROUND: Acute myeloid leukemia (AML) is one of the most common types of leukemia in adults. However, AML is relatively rare in the population overall, accounting for only about 1 percent of all cancers. Treatment for AML can be very effective for some patients, yet it leaves others with serious and even life-threatening side effects. Chemotherapy is still the primary treatment for most AML, but over time, leukemia cells become resistant to chemotherapy drugs. In addition, stem cell transplantation, targeted therapy, and immunotherapy are currently available. At the same time, with the progression of the disease, the patient may have corresponding complications, such as coagulation dysfunction, anemia, granulocytopenia, and repeated infection, so transfusion supportive therapy will be involved in the overall treatment regime. To date, few articles have reported on blood transfusion treatment options for patients with ABO subtypes AML-M2. Blood transfusion therapy is an important supportive treatment for AML-M2, and accurate determination of patients' blood type is one of the most important steps in the treatment process. In this study, we explored blood typing and supportive treatment strategies for a patient with A2 subtype AML-M2 to provide the basis for treatment for all patients. CASE SUMMARY: In order to determine the blood type of the patient, serological and molecular biological methods were used for reference tests, and the genetic background was studied to determine the patient's final blood type and select the appropriate blood products for infusion treatment. According to the results obtained by serological and molecular biological methods, the blood type of the patient was A2 subtype; the genotype was A02/001; the irregular antibody screening was negative, and anti-A1 was found in the plasma. According to the overall treatment plan, active anti-infection, elevated cells, component blood transfusion support, and other rescue and supportive treatments were given, and the patient successfully passed the stage of myelosuppression after chemotherapy. Re-examination of bone marrow smears showed that AL was in complete remission of bone marrow signs, and minimal residual leukemia lesions suggested no cells with obvious abnormal immunophenotype (residual leukemia cells < 10-4). CONCLUSION: The infusion of patients with A2 subtype AML-M2 with A irradiated platelets and O washing red blood cells can meet the needs of clinical treatment.
RESUMEN
OBJECTIVE: To study the change of immune status of umbilical cord mesenchymal stem cells (UCMSC) stimulated by toll like receptor 7 (TLR7) agonist CL264. METHODS: TLR7 specific ligand CL264 was used to stimulate the UCMSC. Flow cytometry was conducted to assay the expression of co-stimulators [human leukocyte antigen (HLA)-E, CD80 and CD86] and surface markers of stem cells (CD29, CD59 and CD90). Quantitative PCR was applied to measure the expression variation of immune-related molecules and stem cell markers. Cell differentiation experiment was used to study the change of differentiation ability of UCMSC upon CL264 stimulation. Peripheral blood mononuclear cells (PBMC) were isolated from healthy human and then cocultured with UCMSC in the presence of CL264. Cytotoxicity assay was used to measure the attack of PBMC to UCMSC. RESULTS: Expression of cotimulatory molecules CD86 and HLA-E were enhanced in UCMSC upon CL264 stimulation. Real-time PCR indicated that many pro-inflammatory molecules [interleukin (IL)-1beta, IL-6, IL-8, IL-10, interferon (IFN)-beta, IFN-gamma, nuclear factor-KB (NF-kappaB), transforming growth factor-beta (TGF-beta)] were induced in the presence of CL264 while the expression of stem cells markers were inhibited [Kruppel-like factor-4 (Klf4), Nestin, SRY-related high-mobility-group-box protein-2 (Sox2), Lin28]. Activation of TLR7 also increased the immune attack of PBMC on UCMSC. Our study also indicated that the treatment of CL264 did not influence the differentiation ability of UCMSC. CONCLUSION: TLR7 agonist CL264 could increase the immunogenicity of UCMSC.
