197 Patients with early stage myelodysplastic syndromes show increased frequency of CD4+CD25high+CD127low regulatory T-cells

Fozza, Claudio; Longu, Francesco; Galleu, Antonio; Contini, Salvatore; Virdis, Patrizia; Bonfigli, Silvana; Longinotti, M

doi:10.1016/s0145-2126(11)70199-0

Cited by 2 publications

(2 citation statements)

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“…Although the interpretation of data remains controversial, a large amount of evidence attributes a decrease in NK cell function to the constant presence of multiple inhibitory signals. Further support comes from in vitro studies of patients with cancer, in whom the activity of NK cells is markedly reduced [24][25][26][27][28]. A considerable amount of new insight also stems from experience gained from HSCT.…”

Section: Hla and Kir In Patients And Controlsmentioning

confidence: 99%

Homozygosity for killer immunoglobin-like receptor haplotype A predicts complete molecular response to treatment with tyrosine kinase inhibitors in chronic myeloid leukemia patients

Nasa

Caocci

Littera

et al. 2013

Experimental Hematology

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Section: Hla and Kir In Patients And Controlsmentioning

confidence: 99%

Homozygosity for killer immunoglobin-like receptor haplotype A predicts complete molecular response to treatment with tyrosine kinase inhibitors in chronic myeloid leukemia patients

Nasa

Caocci

Littera

et al. 2013

Experimental Hematology

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“… identified disease classified (by the revised International Prognostic Scoring system) as very low, low or intermediate risk as being associated with higher rates of RBC alloimmunization. Notably, risk MDS has been described to have increased IL‐17 producing CD4+ T cells and decreased regulatory T cells compared to higher risk disease . The lack of treatment with disease‐modifying therapy has also been identified as a risk factor for RBC alloimmunization .…”

Section: Recipient Disease Considerationsmentioning

confidence: 99%

Recipient factors influencing red blood cell alloimmunization

Hendrickson

2019

ISBT Science Series

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Red blood cell (RBC) alloantibodies develop in a subset of individuals following exposure to non‐self RBCs through transfusion, pregnancy or other activities; these antibodies can lead to difficulty locating compatible RBCs, acute or delayed haemolytic transfusion reactions, or haemolytic disease of the newborn. Alloimmunization is underestimated due in part to antibody evanescence, the random nature of post‐transfusion antibody screens, fragmented medical care and the lack of widespread antibody registries. Factors that influence who will develop detectable alloantibodies are not well understood. Transfusion burden is one risk factor for alloimmunization, though many highly transfused individuals never form alloantibodies despite exposure to many RBC units (and many non‐self blood group antigens). Individuals with sickle‐cell disease (SCD) and myelodysplastic syndrome (MDS) are more likely to form RBC alloantibodies than most other patient populations. Individuals with rheumatologic and other forms of autoimmunity, though not chronically transfused, are also at higher‐than‐average risk of forming RBC alloantibodies. Inflammation, in a broad sense, is one common thread amongst these diagnoses associated with high prevalence rates of RBC alloimmunization. Reductionist murine models support some types of inflammation (including viral‐like stimuli) around the time of RBC exposure as being associated with an increased likelihood of alloantibody formation. Strategies other than transfusion avoidance or extended antigen matching beyond ABO/Rh would be beneficial to prevent new RBC alloantibody formation, especially in patients at highest risk.

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197 Patients with early stage myelodysplastic syndromes show increased frequency of CD4+CD25high+CD127low regulatory T-cells

Cited by 2 publications

References 0 publications

Homozygosity for killer immunoglobin-like receptor haplotype A predicts complete molecular response to treatment with tyrosine kinase inhibitors in chronic myeloid leukemia patients

Homozygosity for killer immunoglobin-like receptor haplotype A predicts complete molecular response to treatment with tyrosine kinase inhibitors in chronic myeloid leukemia patients

Recipient factors influencing red blood cell alloimmunization

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