Chimeric antigen receptor (CAR) T cells provide a promising approach to the treatment of hematologic malignancies and solid tumors. Flow cytometry is a powerful analytical modality, which plays an expanding role in all stages of CAR T therapy, from lymphocyte collection, to CAR T cell manufacturing, to in vivo monitoring of the infused cells and evaluation of their function in the tumor environment. Therefore, a thorough understanding of the new directions is important for designing and implementing CAR T‐related flow cytometry assays in the clinical and investigational settings. However, the speed of new discoveries and the multitude of clinical and preclinical trials make it challenging to keep up to date in this complex field. In this review, we summarize the current state of CAR T therapy, highlight the areas of emergent research, discuss applications of flow cytometry in modern cell therapy, and touch upon several considerations particular to CAR detection and assessing the effectiveness of CAR T therapy.
- Despite rivaroxaban treatment, APCR testing can distinguish FVL-HET from normal patients, rendering indiscriminate FVL DNA testing of all patients on rivaroxaban unnecessary. Free protein S should be tested in patients taking rivaroxaban to exclude hereditary protein S deficiency.
Context.— Apixaban causes a false increase in activated protein C resistance (APCR) ratios and possibly protein S activity. Objective.— To investigate whether this increase can mask a diagnosis of factor V Leiden (FVL) or protein S deficiency in an actual population of patients undergoing apixaban treatment and hypercoagulation testing. Design.— During a 4.5-year period involving 58 patients, we compared the following 4 groups: heterozygous for FVL (FVL-HET)/taking apixaban, wild-type/taking apixaban, heterozygous for FVL/no apixaban, and normal APCR/no apixaban. Patients taking apixaban were also tested for protein S functional activity and free antigen (n = 40). Results.— FVL-HET patients taking apixaban had lower APCR ratios than wild-type patients ( P < .001). Activated protein C resistance in FVL-HET patients taking apixaban fell more than 3 SD below the cutoff of 2.2 at which the laboratory reflexes FVL DNA testing. No cases of FVL were missed despite apixaban. In contrast to rivaroxaban, apixaban did not interfere with the assessment of protein S activity (mean activity 93.9 IU/dL, free antigen 93.1 IU/dL, P = .39). A total 3 of 40 patients (8%) had low free protein S antigen (30, 55, and 57 IU/dL), with correspondingly similar activity results (27, 59, and 52 IU/dL, respectively). Apixaban did not cause a missed diagnosis of protein S deficiency. Conclusions.— Despite apixaban treatment, APCR testing can distinguish FVL-HET from healthy patients, rendering indiscriminate FVL DNA testing of all patients on apixaban unnecessary. Apixaban did not affect protein S activity.
Morphea and EF may be histopathologically distinguished based on helper T-cell subtype polarization. These findings offer novel insight into our understanding of disease pathogenesis and support a role for Th1/Th2 immune regulation and Th17 inhibition in anti-fibrotic therapeutic strategy.
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