Figure 2
Figure 2. Screening questions to determine early vaccination candidacy. Note: B-cell numbers are low in the first 1 to 2 months and normalize during months 3 to 12. B-cell recovery is delayed by at least 6 months after anti-B-cell antibody therapy. Antigen-specific responses are impaired also because of limited capacity to undergo somatic mutation and isotype switch during the first year. Normalization of IgA levels can be indicative of isotype switching and is unaffected by IVIG replacement therapy. CD4 counts are generally <200/μL during the first 3 months. Thereafter, recovery is highly variable, generally >200/μL by 6 to 9 months if age <18 years and no chronic GVHD. Adults with chronic GVHD may take >2 years. For these reasons, some institutions defer vaccination until the peripheral CD4 count is >200/μL and the CD19 (B-cell) count is >20 /μL. Most circulating T cells at year 1 (especially in adults) are memory/effector T cells derived from infused T cells. These cells can respond to antigens encountered by the donor pre-BMT. Naïve T cells that respond to neoantigens are generated only at 6 to 12 months (earlier in young children, later in old adults). Only limited data exist for the settings of unrelated cord blood and haploidentical HCT or after reduced intensity regimens, and so, for the sake of simplicity, the algorithm does not make further adjustments on these bases. The double asterisk (**) indicates that which agents are sufficiently immunosuppressive to prevent effective vaccination has not been studied. Other than the seasonal flu shot, most vaccinations are avoided when BMT recipients are receiving azacytidine, lenalidomide, or rituximab. We tend to still administer vaccines if patients have little or no chronic GVHD and are on kinase inhibitors (eg, imatinb or sorafenib).

Screening questions to determine early vaccination candidacy. Note: B-cell numbers are low in the first 1 to 2 months and normalize during months 3 to 12. B-cell recovery is delayed by at least 6 months after anti-B-cell antibody therapy. Antigen-specific responses are impaired also because of limited capacity to undergo somatic mutation and isotype switch during the first year. Normalization of IgA levels can be indicative of isotype switching and is unaffected by IVIG replacement therapy. CD4 counts are generally <200/μL during the first 3 months. Thereafter, recovery is highly variable, generally >200/μL by 6 to 9 months if age <18 years and no chronic GVHD. Adults with chronic GVHD may take >2 years. For these reasons, some institutions defer vaccination until the peripheral CD4 count is >200/μL and the CD19 (B-cell) count is >20 /μL. Most circulating T cells at year 1 (especially in adults) are memory/effector T cells derived from infused T cells. These cells can respond to antigens encountered by the donor pre-BMT. Naïve T cells that respond to neoantigens are generated only at 6 to 12 months (earlier in young children, later in old adults). Only limited data exist for the settings of unrelated cord blood and haploidentical HCT or after reduced intensity regimens, and so, for the sake of simplicity, the algorithm does not make further adjustments on these bases. The double asterisk (**) indicates that which agents are sufficiently immunosuppressive to prevent effective vaccination has not been studied. Other than the seasonal flu shot, most vaccinations are avoided when BMT recipients are receiving azacytidine, lenalidomide, or rituximab. We tend to still administer vaccines if patients have little or no chronic GVHD and are on kinase inhibitors (eg, imatinb or sorafenib).

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