In recent years, many studies have focused on the abnormality of B-cell immunity as a major factor in the pathogenesis of chronic graft-versus-host disease (cGVHD) after allogeneic hematopoietic stem cell transplantation (HSCT)[1, 2]. Sarantopoulos et al. firstly reported abnormal B-cell homeostasis in the post-transplant environment where naïve B-cell lymphopenia and excessive B-cell activation factor (BAFF) promoted the responsiveness of B cells to antigens, and increased survival of activated B cells [3, 4]. Ensuing studies demonstrated that follicular helper T cells (Tfhs) promoted the differentiation from naïve B cells into germinal center B cells, which may result in the aberrant production of IgG alloantibodies causing tissue damage in cGVHD-target organs [5, 6]. Based on these findings, therapies targeting activated B cells have been developed for patients with cGVHD [7–10]. However, the factors that may be associated with naïve B lymphopenia early after transplant, which could trigger to form the basal pathogenesis of chronic GVHD, have not been well studied.