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. Author manuscript; available in PMC: 2026 Jul 8.
Published in final edited form as: Blood Immunol Cell Ther. 2026 Apr 7;2(2):100042. doi: 10.1016/j.bict.2026.100042

Identification of an optimal absolute lymphocyte count at leukapheresis in patients with lymphoma treated with CART

Kunhwa Kim 1,*, Zachary Hunzeker 1,*, Xiaowen Sun 1, Ryan Sun 1, Timothy Voorhees 2, Youssef Youssef 2, Narendranath Epperla 2, Michelly De Castro 1, Karla Ow 1, Minifrida Santiago 1, Jaimole Varghese 1, Amy Ayers 1, Jeremy Ramdial 1, Chitra Hosing 1, Partow Kebriaei 1, Elizabeth Shpall 1, Michael Jain 3, Julio Chavez 3, Frederick L Locke 3, Sattva S Neelapu 1, Sairah Ahmed 1, Paolo Strati 1
PMCID: PMC13340592  NIHMSID: NIHMS2191126  PMID: 42416925

Abstract

T-cell fitness can be impaired in patients with large B-cell lymphoma (LBCL) planned for CART (chimeric antigen receptor T-cell therapy). Although absolute lymphocyte count (ALC) at the time of leukapheresis has been shown to associate with outcomes in patients with LBCL treated axicabtagene ciloleucel (axi-cel), no threshold has been identified. This is a multicenter retrospective study including 1 axi-cel training and validation cohort, and 1 mixed-product validation cohort. The change-point method was used to identify an ALC threshold associating with optimal progression-free survival (PFS). Three hundred seventy-nine patients were included in the axi-cel training cohort. ALC as a continuous variable was associated with complete response on day 30 (median, 0.79 × 103/μL vs 0.63 × 103/μL; P = .004). An ALC of 0.34 × 103/μL was identified as the optimal threshold for PFS (7 vs 3 months; P = .0013). The association was confirmed in the axi-cel validation cohort (165 patients; 19.8 vs 3.5 months; P = .04) but not in the mixed validation cohort (163 patients; 5 vs 1.5 months; P = .3). On univariate analysis, characteristics associated with ALC above the threshold included low International Prognostic Index score (P = .02), low serum C-reactive protein level (P = .02), low serum ferritin level (P < .001), and low number of prior lines of systemic therapy (P = .02). An ALC of >0.34 × 103/μL at the time of apheresis is associated with optimal outcomes in patients with LBCL treated with axi-cel. A deeper investigation of the impact of prior therapies on the number and phenotype of lymphocytes at time of apheresis is warranted.

Introduction

Chimeric antigen receptor (CAR) T-cell therapy (CART) has become a mainstay treatment for patients with relapsed or refractory large B-cell lymphoma (LBCL) since its initial US Food and Drug Administration approval in 2017, along with expanding indications that hold promise for its curative potential.1–3 Despite these advances, ~50% to 60% of patients experience relapsed or refractory disease with poor prognosis.1 Therefore, CART optimization remains critically important to improve clinical outcomes.

In this regard, T-cell fitness in the infusion product and peripheral blood has emerged as one of the key factors influencing CAR T-cell efficacy because this treatment uses patients’ autologous T cells.4–6 Different variables, including prior therapies (such as bendamustine), use of immunosuppressive agents, age, comorbidities, and disease burden, can impair T-cell function and negatively affect treatment outcomes.4,7 Therefore, identifying biomarkers of T-cell fitness at the time of leukapheresis is essential to guide optimal treatment timing and patient selection, and absolute lymphocyte counts (ALC) may serve as a simple and quantitative surrogate marker. Interestingly, ALC and its kinetics have shown to associate with CAR T-cell efficacy in patients with LBCL treated with axicabtagene ciloleucel (axi-cel),8–10 and an arbitrary threshold of 0.1 × 103/μL is typically used to at the time of apheresis to proceed with leukocyte collection.

However, no specific ALC thresholds have been identified to allow optimal timing of leukapheresis in patients with LBCL planned for axi-cel, and the prognostic role of ALC for other products remains unknown.

Methods

Patient selection and assessment

This is a retrospective cohort analysis of patients with relapsed or refractory LBCL treated with standard-of-care (SOC) CART in second-line or beyond at 3 different academic centers, including 1 training cohort and 2 validation cohorts. SOC was defined as the administration of commercial product outside of a clinical trial. The training cohort included patients with LBCL who received SOC axi-cel at The University of Texas MD Anderson Cancer Center between January 2018 and September 2023 (data cutoff: March 2024). The 2 validation cohorts were as follows: (1) patients treated with SOC axi-cel at the Moffit Cancer Center between January 2018 and September 2023 (data cutoff: 30 March 2024) and (2) patients treated with axi-cel or tisagenlecleucel (tisa-cel) at The Ohio State University James Comprehensive Cancer Center between January 2018 and January 2023 (data cutoff: February 2024).

This study was approved by the institutional review board of each academic center and conducted in accordance with individual institutional guidelines and the principles of the Declaration of Helsinki. Baseline characteristics for all patients were collected on the day of leukapheresis. Cytokine release syndrome (CRS) and immune effector cell–associated neurotoxicity syndrome (ICANS) were graded for up to 30 days after CART infusion according to the CARTOX grading system from January 2018 to April 2019 and according to the American Society for Transplantation and Cellular Therapy (ASTCT) criteria from May 2019 onward.11,12 Performance status was defined according to the Eastern Cooperative Oncology Group, and the International Prognostic Index (IPI) score was calculated as previously reported.13,14 Response status was determined by positron emission tomography–computed tomography according to the Lugano 2014 criteria.15 At all 3 centers, patients had no exposure to systemic corticosteroids for 7 days or to systemic antitumoral therapy for 14 days before leukapheresis, in addition to an ALC preferably of at least 0.1 × 103/μL to be proceed with collection.

Statistical methods

Association between categorical variables was evaluated using a χ2 test or Fisher exact test. Differences in continuous variables between patient groups were evaluated by the Mann-Whitney U test. Progression-free survival (PFS) was defined as the time from the start of CART infusion to progression of disease, death, or last follow-up (whichever occurred first). Overall survival was defined as the time from the start of CART infusion to death or last follow-up. PFS and overall survival at specific time points were calculated for all patients in the study and for the subgroups of patients using Kaplan-Meier estimates and were compared between subgroups using the log-rank test. Only factors significant (P ≤ .05) on univariate analysis were included in multivariate models. The maximally selected log-rank statistic (also known as change-point method) was used to determine the optimal ALC threshold at the time of leukapheresis associated with PFS.16 Statistical analyses were completed using SPSS 24, GraphPad Prism 8, and R version 4.1.1.

Results

Patient characteristics

Seven hundred nine patients were included in the analysis: 379 in the axi-cel training cohort, 165 in the axi-cel validation cohort, and 165 in the mixed validation cohort. In the mixed validation cohort, 92 (56%) patients received tisa-cel and 71 (43%) received axi-cel.

In the axi-cel training cohort, at the time of leukapheresis, median age was 61 years (range, 18–85), 260 (69%) were male, and the median number of prior lines of systemic therapy was 3 (range, 1–15). A total of 220 (58%) had an IPI score of 3 to 5, and 238 (63%) had lactate dehydrogenase above the upper limit of normal. Baseline characteristics at the time of leukapheresis for all 3 cohorts are summarized in Table 1. Notably, patients in the axi-cel training cohort had a higher median number of prior lines of systemic therapies (3 vs 2 each) and a higher rate of patients with an IPI score of 3 to 5 than those in the axi-cel validation and mixed validation cohorts (58% vs 40% and 47%, respectively). Only 1% of patients in each cohort did not reach the preferred ALC threshold at leukapheresis (ie, 0.1 × 103/μL).

Table 1.

Baseline characteristics at the time of leukapheresis

n (%) or median (range)
Patients (N = 709) Axi-cel training cohort (n = 379) Axi-cel validation cohort (n = 165) Mixed validation cohort (n = 163)
Age, y 61 (18–85) 64 (19–80) 63 (23–88)
Male 260 (69) 99 (60) 96 (58)
ECOG performance status 3–4 53 (14) 6 (4) 16 (9.7)
Prior systemic therapies, n 3 (1–15) 2 (1–7) 2 (1–7)
IPI score 3–5 220 (58) 66 (40) 78 (47)
LDH level above upper normal limit 238 (63) 110 (67) 100 (61)
Refractory disease 284 (75) 127 (77) 86 (53)
Previous autologous SCT 62 (16) 27 (16) 38 (24)
Previous allogeneic SCT 7 (2) 2 (1) 2 (1)
ALC, 103/μL 0.71 (0.05–4.51) 0.61 (0.05–3.63) 0.77 (0.07–5.01)
C-reactive protein level, mg/L 10.17 (0.26–1 422) 14.10 (0.30–261) 16.00 (0.73–1 646)
Ferritin level, ng/mL 500 (13–14 180) 437 (16–4740) 469 (23–22 220)
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ECOG, Eastern Cooperative Oncology Group; LDH, lactate dehydrogenase; SCT, stem cell transplant.

Association between ALC as continuous variable and clinical outcomes

In the axi-cel training cohort, median ALC at the time of leukapheresis was 0.71 × 103/μL (range, 0.05–4.51). During the first 30 days after axi-cel infusion, CRS of any grade was observed in 350 (92%) patients and ICANS of any grade in 223 (59%). On day 30, 202 (53%) had achieved a complete response on restaging positron emission tomography–computed tomography.

No association was observed between ALC as a continuous variable and CRS of any grade (median, 0.63 × 103/μL vs 0.72 × 103/μL; P = .96) or ICANS of any grade (median, 0.70 × 103/μL vs 0.71 × 103/μL; P = .91). However, a significantly higher ALC was observed in patients who achieved complete response on day 30 than in those who did not (median, 0.79 × 103/μL vs 0.63 × 103/μL; P = .004; Figure 1).

Figure 1. Association between ALC as a continuous variable and day 30 CR in the axi-cel training cohort.

Figure 1.

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ALC, absolute lymphocyte count; CR, complete response; CR30, day 30 CR.

Identification of an optimal ALC threshold at the time of leukapheresis

In the axi-cel training cohort, after a median follow-up of 19 months (95% confidence interval, 15–24), 247 (65%) patients progressed and/or died, with a median PFS of 6 months (95% confidence interval, 4–7). Using the change-point method, an ALC of 0.34 × 103/μL at the time of leukapheresis was identified as the optimal threshold for PFS, and 306 (81%) patients with levels >0.34 × 103/μL experienced a significantly longer PFS (median, 7 vs 3 months; P = .0013) (Figure 2). The association between ALC and PFS was also maintained in multiple bivariate Cox proportional hazards analyses, including ALC threshold and the following variables: IPI score, number of prior lines of systemic therapy, lactate dehydrogenase serum levels, C-reactive protein serum levels, ferritin serum levels, and previously refractory disease.

Figure 2. Association between optimal ALC threshold and PFS in the axi-cel training cohort.

Figure 2.

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The optimal ALC threshold was 0.34 × 103/μL. LK.ALC, absolute lymphocyte count.

On univariate analysis, baseline characteristics at the time of leukapheresis that were associated with ALC above the threshold were as follows: low (0–2) IPI score (30% vs 44%; P = .02), low serum C-reactive protein level (median, 15.9 vs 9.0 mg/L; P = .02), low serum ferritin level (median, 801 vs 428 ng/mL; P < .001), and low number of prior lines of systemic therapy (median, 3 vs 2; P = .02).

Validation in the axi-cel and mixed external cohort

Similarly to what was observed in the axi-cel training cohort, in the axi-cel validation cohort (n = 165), patients with an ALC at leukapheresis of 0.34 × 103/μL or higher (n = 130) experienced a significantly longer PFS than those with ALC below the threshold (n = 35), with a median PFS of 19.8 months compared with that of 3.5 months (P = .04; Figure 3A). In contrast, in the mixed validation cohort (n = 163), patients with an ALC of >0.34 × 103/μL at the time of leukapheresis (n = 146) experienced a similar PFS as for those with ALC below the threshold (n = 17), with a median PFS of 5 months compared with that of 1.5 months (P = .3; Figure 3B).

Figure 3. Association between PFS and ALC threshold in the validation cohorts.

Figure 3.

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(A) Axi-cel validation cohort; (B) mixed validation cohort. CI, confidence interval; KM, Kaplan-Meier.

Discussion

This large multicenter retrospective study identified, through a training and 2 validation cohorts, that an ALC threshold of 0.34 × 103/μL at the time of leukapheresis was associated with improved PFS in patients with LBCL treated with axi-cel. These findings suggest that ALC serves as a simplified and informative laboratory parameter to guide the optimal timing of apheresis for patients receiving this specific CART product.

CART efficacy has shown to be closely related to T-cell biology, and memory subsets have demonstrated significant ex vivo expansion, persistence, and antitumoral activity.5 However, less differentiated T-cell subsets, including naïve, early memory T cells, and central memory T cells, have also shown to be associated with improved post-CART outcomes in LBCL and other hematologic malignancies.11,12,14,15 In this regard, in ZUMA-7, a higher proportion of the naïve T-cell phenotype (CCR7+ CD45RA+) with the expression of CD27 and CD28 associated with more durable responses decreased rates of CRS or ICANS compared with a higher proportion of more differentiated, memory effector T cells (CCR7− CD45RA−).

Although accurate measurement and biological characterization of T-cell fitness are crucial, they are not widely and immediately available in clinical practice, and simple laboratory parameters, such as ALC, may be used as surrogate markers. In this regard, in a retrospective study including 50 patients with LBCL treated with axi-cel, a B-cell proportion of ≥0.5% and a ratio of ALC to absolute monocyte count ≥1.2 at the time of leukapheresis was associated with improved PFS; and the findings were validated in a cohort of 99 patients with LBCL treated in ZUMA-1.17 Interestingly, ALC at the time of leukapheresis was also associated with favorable post-CART outcomes in patients with multiple myeloma.18–20

In our study, a lower number of prior lines of systemic therapies and lower levels of markers of disease burden and inflammation were associated with a higher ALC threshold at the time of leukapheresis. Although a lower number of prior lines of systemic therapy identifies a more favorable timing and a potentially less aggressive disease, it has also shown to associate with higher proportions of naïve T-cell subsets.21 Accordingly, in ZUMA-7, patients who received axi-cel in second-line had a median PFS of 14.7 months, whereas those who received it in third-line in the standard arm experienced a median PFS at 6.3 months.22 ,23 Notably, patients with LBCL who undergo earlier and preemptive leukapheresis have shown to exhibit higher proportions of naïve T cells than those who undergo leukapheresis later.24 In addition, tumor burden and related immune suppression have been shown to associate with poor post-CART outcomes.25 Although CART is moving to earlier lines of therapy and preemptive leukapheresis could occur in the near future, a better understanding of the association between number, type and timing of prior lines of therapy, and ALC at time of leukapheresis could improve outcomes in the present therapeutic landscape.

In our study, the association between ALC at leukapheresis and outcomes applied only to the axi-cel training and validation cohort, but not the mixed validation cohort. The CD28 costimulatory domain used for axi-cel promotes effector memory T-cell differentiation, whereas the 4–1BB costimulatory domain used for tisa-cel and liso-cel has shown to promote the development of central memory-like T cells through distinct metabolic programming.26 Although these biological differences may be responsible for the observed clinical outcomes, large data sets of liso-cel–treated patients and functional analyses are needed. In addition, only 17 patients had ALC below the threshold in the mixed validation cohort, and negative findings in patients treated with products other than axi-cel should be taken with caution. In this regard, we acknowledge multiple limitations of this study, including its retrospective nature, its population heterogeneity, and the lack of patients treated with liso-cel. We also acknowledge that, although clinically practical, dichotomizing a continuous variable such as ALC may oversimplify risk stratification and that expected analytical variability in ALC measurement may weaken the clinical applicability of a specific threshold. In conclusion, an ALC threshold of 0.34 × 103/μL at the time of leukapheresis can help identify patients with LBCL who may derive the greatest benefit from axi-cel and those who may require alternative therapeutic strategies. Based on our data, this does not apply to tisa-cel and needs further investigation with liso-cel. A prospective validation of our findings and a deeper biological characterization of T cells at the time of leukapheresis and their association with prior therapies are warranted. Simultaneously, patients should not delay leukapheresis until reaching a certain ALC threshold but rather be advised on its potential biological and clinical significance and on its potential impact on subsequent outcomes.

Key Points.

  • An ALC of 0.34 × 103/μL at the time of leukapheresis is associated with improved PFS in patients with LBCL treated with axi-cel.

  • The number of lines of systemic therapy, along with markers of disease burden and inflammation, are associated with ALC at leukapheresis.

Acknowledgments

This research is supported, in part, by The University of Texas MD Anderson Cancer Center Support Grant from the National Cancer Institute, National Institutes of Health (P30 CA016672). The MD Anderson Lymphoma Tissue Bank was used in this study and is supported by KW Cares. P.S. is supported by the Leukemia Lymphoma Society Scholar Clinical Research Career Development Program.

Conflict-of-interest disclosure:

P.S. is a consultant/has served on advisory boards for Roche-Genentech, AbbVie-Genmab, Ipsen, Kite/Gilead, Novartis, Incyte, Lilly, AstraZeneca-Acerta, BeOne, ADC Therapeutics, and Sobi; and has received research funds from Sobi, AstraZeneca-Acerta, ALX Oncology, and ADC Therapeutics. T.V. is a consultant/has served on advisory boards for Genmab/AbbVie, ADC Therapeutics, Novartis, and Recordati; and received research support from Kite, Incyte/MorphoSys, Genmab/AbbVie, and Recordati. S.S.N. received research support from Kite/Gilead, Bristol Myers Squibb (BMS), Allogene, Precision Biosciences, Adicet Bio, and Sana Biotechnology; served as an advisory board member/consultant for Kite/Gilead, Merck, Sellas Life Sciences, Athenex, Allogene, Incyte, Adicet Bio, BMS, bluebird bio, Fosun Kite, Sana Biotechnology, Caribou, Astellas Pharma, MorphoSys, Janssen, Chimagen, ImmunoACT, Orna Therapeutics, Takeda, and Synthekine; has stock options in Longbow Immunotherapy, Inc; and has intellectual property related to cell therapy. F.L.L. is a consultant/has served on advisory boards for A2, Adaptive Biotechnologies, Adaptimmune, Allogene, Amgen, AstraZeneca, bluebird bio, BMS, Calibr, Caribou, EcoR1, Gerson Lehrman Group, Iovance, Kite Pharma, Janssen, Legend Biotech, Miltenyi, Novartis, Sana, Pfizer, and Poseida; and has intellectual property related to cell therapy. E.J.S. is a consultant/has served on advisory boards for the New York Blood Center, Adaptimmune, Navan, Celaid Therapeutics, Zelluna Immunotherapy, FibroBiologics, Axio, and Orca Biosystems; and has license agreements with Takeda, Affimed, and Prana X. K.K. has become an employee for Pfizer after the completion of this project. M.J. is a consultant/has served on advisory boards for Kite/Gilead, Janssen, Arcellx, BMS, Abbvie, and Legend; has received honoraria from Prime Education, OncLive, Decera, and Curio Science; has equity with Pagona Health; and has received research funds from Kite/Gilead, Lilly, and Incyte. The remaining authors declare no competing financial interests.

The data that support the findings of this study are available from the corresponding author, Paolo Strati (pstrati@mdanderson.org), upon reasonable request.

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