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Some patients with acute myeloid leukemia (AML) may have trouble with immunotherapy following chemotherapy. Researchers from the National Heart, Lung and Blood Institute may have found a reason why.
Related: Novel Treatment Shows Promise for Acute Lymphoblastic Leukemia
The researchers wanted to perform a “deep assessment” of the state of the adaptive immune system in AML patients in remission after chemotherapy. They used these patients’ response to seasonal influenza vaccination as a surrogate for the robustness of the immune system. The researchers say their approach was unique in that they established a comprehensive picture of the adaptive “immunome” by simultaneously examining the genetic, phenotypic, and functional consequences of chemotherapy.
Their assessment revealed a “dramatic impact” in the B-cell compartment, which appeared slower to recover than the T-cell compartment. Of 10 patients in the study, only 2 generated protective titers in response to vaccination. Most had abnormal frequencies of transitional and memory B-cells. The researchers say the inability of AML patients to produce protective antibody titers in response to influenza vaccination is likely due to multiple B-cell abnormalities.
Related: Six Open Clinical Trials That Are Expanding Our Understanding of Immunotherapies
The researchers “strikingly” found similar patterns of immune dysfunction across all the patients in the study. When they ranked patients based on time elapsed since chemotherapy, the degree of dysfunction was shown to be less in patients who had the most time elapsed form their chemotherapy treatment.
The researchers conclude the “consistent finding” of a reduction of memory B-cells in all the AML patients suggests that humoral immunity reconstitution is “a very long process.” They add that a better understanding of the changes in adaptive immune cell subsets after chemotherapy will be useful in designing immunotherapies that can work with existing immune capacity.
Source:
Goswami M, Prince G, Biancotto A, et al. J Transl Med. 2017;15:155.
doi: 10.1186/s12967-017-1252-2
Some patients with acute myeloid leukemia (AML) may have trouble with immunotherapy following chemotherapy. Researchers from the National Heart, Lung and Blood Institute may have found a reason why.
Related: Novel Treatment Shows Promise for Acute Lymphoblastic Leukemia
The researchers wanted to perform a “deep assessment” of the state of the adaptive immune system in AML patients in remission after chemotherapy. They used these patients’ response to seasonal influenza vaccination as a surrogate for the robustness of the immune system. The researchers say their approach was unique in that they established a comprehensive picture of the adaptive “immunome” by simultaneously examining the genetic, phenotypic, and functional consequences of chemotherapy.
Their assessment revealed a “dramatic impact” in the B-cell compartment, which appeared slower to recover than the T-cell compartment. Of 10 patients in the study, only 2 generated protective titers in response to vaccination. Most had abnormal frequencies of transitional and memory B-cells. The researchers say the inability of AML patients to produce protective antibody titers in response to influenza vaccination is likely due to multiple B-cell abnormalities.
Related: Six Open Clinical Trials That Are Expanding Our Understanding of Immunotherapies
The researchers “strikingly” found similar patterns of immune dysfunction across all the patients in the study. When they ranked patients based on time elapsed since chemotherapy, the degree of dysfunction was shown to be less in patients who had the most time elapsed form their chemotherapy treatment.
The researchers conclude the “consistent finding” of a reduction of memory B-cells in all the AML patients suggests that humoral immunity reconstitution is “a very long process.” They add that a better understanding of the changes in adaptive immune cell subsets after chemotherapy will be useful in designing immunotherapies that can work with existing immune capacity.
Source:
Goswami M, Prince G, Biancotto A, et al. J Transl Med. 2017;15:155.
doi: 10.1186/s12967-017-1252-2
Some patients with acute myeloid leukemia (AML) may have trouble with immunotherapy following chemotherapy. Researchers from the National Heart, Lung and Blood Institute may have found a reason why.
Related: Novel Treatment Shows Promise for Acute Lymphoblastic Leukemia
The researchers wanted to perform a “deep assessment” of the state of the adaptive immune system in AML patients in remission after chemotherapy. They used these patients’ response to seasonal influenza vaccination as a surrogate for the robustness of the immune system. The researchers say their approach was unique in that they established a comprehensive picture of the adaptive “immunome” by simultaneously examining the genetic, phenotypic, and functional consequences of chemotherapy.
Their assessment revealed a “dramatic impact” in the B-cell compartment, which appeared slower to recover than the T-cell compartment. Of 10 patients in the study, only 2 generated protective titers in response to vaccination. Most had abnormal frequencies of transitional and memory B-cells. The researchers say the inability of AML patients to produce protective antibody titers in response to influenza vaccination is likely due to multiple B-cell abnormalities.
Related: Six Open Clinical Trials That Are Expanding Our Understanding of Immunotherapies
The researchers “strikingly” found similar patterns of immune dysfunction across all the patients in the study. When they ranked patients based on time elapsed since chemotherapy, the degree of dysfunction was shown to be less in patients who had the most time elapsed form their chemotherapy treatment.
The researchers conclude the “consistent finding” of a reduction of memory B-cells in all the AML patients suggests that humoral immunity reconstitution is “a very long process.” They add that a better understanding of the changes in adaptive immune cell subsets after chemotherapy will be useful in designing immunotherapies that can work with existing immune capacity.
Source:
Goswami M, Prince G, Biancotto A, et al. J Transl Med. 2017;15:155.
doi: 10.1186/s12967-017-1252-2