Figure 2.
Immune recovery of the main cell subsets is positively or negatively influenced by different pre- and post-HCT factors and the subsets are interconnected. Recovery of CD4+ T cells is negatively affected by excessive exposure to ATG/ATLG and by immune suppressive GVHD therapies. Conversely, young donor age and use of PBSC as source for HCT hasten CD4+ T-cell recovery. Specific graft manipulations and underlying diseases can variably augment or hinder CD4+ T-cell IR. ATG/ATLG also impairs CD8+ T-cell recovery, along with using CB as a graft source,12 likely due to the naivety of CB CD8+ T cells. The use of PBSC may hasten recovery of CD8+ T-cell IR. The impact of viral reactivations and GVHD remains to be fully characterized. Although higher numbers of CD8+ T cells may offer protection against viral reactivation, this may also indicate an already active antiviral response and/or alloimmunity.13 As for GVHD, the correlation with CD8+ counts is also not established but in some studies increased CD8+ T-cell counts were observed in patients who have ongoing aGVHD1 or cGVHD.12,14 ATG/ATLG exposure or use of PTCy can delay recovery of NK cells, whereas use of CB or ex vivo TCD promotes early NK cell recovery.15-18 In 1 retrospective cohort study of 499 patients, median numbers of NK cells at 1 month after HCT were reduced after PTCy (20 cells per μL), when compared with ATLG (79-113 cells per μL) or neither PTCy nor ATLG (210 cells per μL). These differences failed to persist after 2 months after HCT.18 Older recipient age has been associated with poorer B-cell IR, as well as use of rituximab, or TBI, which can lead to long-term B-cell defects characterized by lower naïve B cells and switched memory B cells for up to 2 years after HCT.19,20 B-cell IR is faster after HCT with CB or after PTCy. Several studies indicate an interconnection among recovery of different lymphocyte subsets that needs better characterization.13,21 ATLG, anti–T lymphoglobulin; CB, cord blood; PBSC, peripheral blood stem cell; TBI, total body irradiation.

Immune recovery of the main cell subsets is positively or negatively influenced by different pre- and post-HCT factors and the subsets are interconnected. Recovery of CD4+ T cells is negatively affected by excessive exposure to ATG/ATLG and by immune suppressive GVHD therapies. Conversely, young donor age and use of PBSC as source for HCT hasten CD4+ T-cell recovery. Specific graft manipulations and underlying diseases can variably augment or hinder CD4+ T-cell IR. ATG/ATLG also impairs CD8+ T-cell recovery, along with using CB as a graft source,12 likely due to the naivety of CB CD8+ T cells. The use of PBSC may hasten recovery of CD8+ T-cell IR. The impact of viral reactivations and GVHD remains to be fully characterized. Although higher numbers of CD8+ T cells may offer protection against viral reactivation, this may also indicate an already active antiviral response and/or alloimmunity.13 As for GVHD, the correlation with CD8+ counts is also not established but in some studies increased CD8+ T-cell counts were observed in patients who have ongoing aGVHD1 or cGVHD.12,14 ATG/ATLG exposure or use of PTCy can delay recovery of NK cells, whereas use of CB or ex vivo TCD promotes early NK cell recovery.15-18 In 1 retrospective cohort study of 499 patients, median numbers of NK cells at 1 month after HCT were reduced after PTCy (20 cells per μL), when compared with ATLG (79-113 cells per μL) or neither PTCy nor ATLG (210 cells per μL). These differences failed to persist after 2 months after HCT.18 Older recipient age has been associated with poorer B-cell IR, as well as use of rituximab, or TBI, which can lead to long-term B-cell defects characterized by lower naïve B cells and switched memory B cells for up to 2 years after HCT.19,20 B-cell IR is faster after HCT with CB or after PTCy. Several studies indicate an interconnection among recovery of different lymphocyte subsets that needs better characterization.13,21 ATLG, anti–T lymphoglobulin; CB, cord blood; PBSC, peripheral blood stem cell; TBI, total body irradiation.

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