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A Syngeneic Mouse B-Cell Lymphoma Model for Pre-Clinical Evaluation of CD19 CAR T Cells
Published on: October 16, 2018
Cutaneous B-cell lymphoma with loss of CD20 immunoreactivity after rituximab therapy
Loren E Clarke1, Michael G Bayerl, W Christopher Ehmann
1Department of Pathology, The Pennsylvania State University College of Medicine/Hershey Medical Center, C7633 Hershey Medical Center (H083/Box 850), Hershey, PA 17033, USA. lclarke816@aol.com
Insights
Loss of CD20 expression in B-cell lymphomas can occur after rituximab therapy, leading to CD20-negative relapses. Immunohistochemistry for CD79a is crucial for identifying these CD20-negative B-cell lymphomas.
Area of Science:
- Hematology
- Oncology
- Immunology
Background:
- CD20 is a B-cell specific antigen crucial for identifying B-cell lymphomas, with ~95% being CD20-positive.
- Anti-CD20 monoclonal antibodies like rituximab are standard therapies for CD20-positive B-cell lymphomas.
Observation:
- A patient with CD20-positive systemic B-cell lymphoma experienced a relapse with CD20-negative cutaneous involvement after rituximab treatment.
- Skin biopsy revealed an atypical lymphocytic infiltrate negative for CD20 but positive for CD45rb (LCA) and CD79a.
Findings:
- Loss of CD20 expression is a mechanism of relapse in B-cell lymphomas treated with rituximab.
- CD79a serves as a reliable marker for identifying CD20-negative B-cell lymphomas, aiding in diagnosis.
Implications:
- Recognizing CD20-negative B-cell lymphoma is vital for appropriate patient management.
- Increased use of rituximab may lead to a higher incidence of CD20-negative relapses.
- CD79a immunohistochemistry is essential for diagnosing CD20-negative B-cell lymphomas.
Background:
Antibodies to the B-cell-specific antigen CD20 are widely used for immunohistochemical identification of B-cell lymphomas, approximately 95% of which are strongly CD20-positive.
Methods:
We report a 51-year-old male with a CD20-positive systemic B-cell lymphoma who developed a CD20-negative relapse with secondary cutaneous involvement after therapy with the anti-CD20 monoclonal antibody rituximab (Rituxan).
Results:
Biopsy of a skin nodule demonstrated an atypical lymphocytic infiltrate that was negative for CD20, CD3, lysozyme, and myeloperoxidase, but strongly positive for CD45rb (LCA) and the B-cell marker CD79a.
Conclusions:
We conclude that loss of CD20 expression in cutaneous B-cell lymphoma (both primary and secondary) is important to recognize, that immunohistochemistry for CD79a, another widely expressed B-cell marker, is useful in the identification of CD20-negative B cells in such cases, and that loss of CD20 expression may become more common, as use of rituximab is expected to increase.

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