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The field is now evolving through novel strategies, including bispecific CAR-T cells targeting CD19 and CD22, as well as CD38-specific CAR-T cells, which aim to increase therapeutic efficacy by countering mechanisms such as antigen escape [68, 69]
In contrast, inhibition of CD38 exoenzymatic activity using the Ab68 mAb reduced the production of ADPR (43)
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UV damage, pollutants and environmental stressors lead to a breakdown of collagen and elastin in skin
