ArticleFrontiers in immunology2026
Type-II-CD20-targeted therapy for CD38 antibody-refractory antibody-mediated rejection after kidney transplantation: a case report.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
With the advent of CD38 antibody therapy, an effective treatment option for antibody-mediated rejection (ABMR) appears achievable. However, a subset of patients remains refractory. We report a kidney transplant recipient with persistent microvascular inflammation in kidney allograft biopsy after six months of CD38 antibody treatment, necessitating rescue therapy. Persistent detection of peripheral CD38-negative class-switched memory B cells prompted additional deep B-cell depletion using a humanized, glycoengineered, IgG1 monoclonal antibody targeting the type-II epitope of CD20. Follow-up kidney biopsy demonstrated histological resolution of microvascular inflammation, while normalization of donor-derived cell-free DNA was consistent with remission of ABMR. In this case of CD38 antibody-refractory ABMR, adjunctive type-II-CD20 antibody therapy had a favorable response. This highlights the potential contribution of additional effector cells to refractory ABMR, such as CD38-negative class-switched memory B cells. These findings suggest a potential role for individualized, multimodal B-cell-directed immunomodulatory strategies that may improve outcomes in selected patients with treatment-refractory ABMR, thus contributing to sustained allograft survival.
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