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Selective lymphodepletion underlies the efficacy of horse anti-thymocyte globulin-based immunosuppressive therapy in aplastic anemia

Title: Selective lymphodepletion underlies the efficacy of horse anti-thymocyte globulin-based immunosuppressive therapy in aplastic anemia
Authors: Emma S. Pool; Cilia R. Pothast; Shannah M. Gennesse; Esther H.M. van Egmond; Julia M. Giezen; Sabrina A.J. Veld; René E.M. Toes; Frits Koning; Constantijn J.M. Halkes; Mirjam H.M. Heemskerk; Dirk Jan A.R. Moes; Jennifer M-L. Tjon
Source: Haematologica, Vol 999, Iss 1 (2026)
Publisher Information: Ferrata Storti Foundation
Publication Year: 2026
Collection: Directory of Open Access Journals: DOAJ Articles
Subject Terms: Diseases of the blood and blood-forming organs; RC633-647.5
Description: Horse-derived anti-thymocyte globulin (ATGAM) in combination with long-term ciclosporin is the first-line treatment for most immune-mediated aplastic anemia (AA) patients. The exact impact of this immunosuppressive therapy (IST) on hematological recovery and the immune landscape, however, remains poorly understood. We report a longitudinal analysis of the pharmacodynamic effects of ATGAM-based IST in a cohort of 44 AA patients. With flow cytometry we quantified plasma levels of lymphocyte-binding ATGAM, which is believed to mediate the therapeutic effect. Population pharmacokinetic modeling revealed substantial between-patient variability in ATGAM exposure, with higher exposure levels associating to earlier hematologic recovery. ATGAM bound all lymphoid lineages and profoundly depleted Tand NK-cells at high plasma concentrations. Strikingly, ATGAM did not deplete B-cells but instead induced an increase of CD27+ B-cells. Deep immunophenotyping on series of peripheral blood samples collected up to three years after start of IST demonstrated that ATGAM induced rapid depletion of T-cells, including KLRG1+ terminally differentiated CD8+ Tcells and Th17-like CCR6+CD4+ T-cells. Although naïve and pathogen-specific T-cells were also depleted, they recovered quickly, indicating preservation of protective immunity. Notably, CCR6++ B-cells, implicated in AA pathogenesis, escaped ATGAM depletion but reduced gradually over time along with residual potentially pathogenic T-cells, including the CCR6+CD4+ T-cells. This could explain the crucial contribution of long-term ciclosporin to successful IST. Collectively, our results identify ATGAM exposure as a factor influencing hematologic recovery, and indicate that the therapeutic effect of IST goes beyond total lymphodepletion but is rather the result of selective depletion and suppression of key lymphocyte subpopulations.
Document Type: article in journal/newspaper
Language: English
Relation: https://haematologica.org/article/view/13129; https://doaj.org/toc/0390-6078; https://doaj.org/toc/1592-8721; https://doaj.org/article/331b188a61df4b2fb667bb6f66bd6958
DOI: 10.3324/haematol.2025.300002
Availability: https://doi.org/10.3324/haematol.2025.300002; https://doaj.org/article/331b188a61df4b2fb667bb6f66bd6958
Accession Number: edsbas.933F317B
Database: BASE