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Published on: February 17, 2022
New-Onset Sarcoidosis During B-cell Maturation Antigen (BCMA)-Directed T-cell Engager Therapy With Teclistamab in
Stefan A Longobardi1, Shoon Oo2, Manpreet Saini3
1Department of Internal Medicine, University of Arkansas for Medical Sciences, Little Rock, USA.
Teclistamab is a bispecific T-cell engager targeting the B-cell maturation antigen (BCMA) on myeloma cells and CD3 on T cells, leading to potent immune activation and durable responses in relapsed/refractory multiple myeloma. Although many immune-mediated complications have been described with teclistamab, granulomatous inflammation or sarcoidosis has not been associated. We present a patient with relapsed/refractory multiple myeloma receiving teclistamab who developed new hypermetabolic lymphadenopathy on positron emission tomography/computed tomography six months after therapy initiation. The patient was asymptomatic with normal pulmonary function, borderline-elevated angiotensin-converting enzyme (ACE) levels, and mild hypercalcemia. Lymph node biopsy revealed nonnecrotizing granulomas without evidence of myeloma or infection. Extensive evaluation excluded fungal, mycobacterial, and opportunistic pathogens. Given clinical stability and sustained myeloma remission, teclistamab was continued without corticosteroid therapy. The patient remained asymptomatic with stable radiographic findings on follow-up. This represents the first reported case of sarcoidosis developing during teclistamab therapy. Recognition of this phenomenon is essential to prevent misinterpretation as myeloma progression or infectious lymphadenitis-diagnostic pitfalls that may lead to unnecessary treatment changes. This case underscores the need for heightened pharmacovigilance, systematic reporting of granulomatous toxicities associated with BCMA-directed therapies, and future immune profiling to identify patients at risk of atypical immune-mediated adverse events.
Teclistamab is a bispecific T-cell engager targeting the B-cell maturation antigen (BCMA) on myeloma cells and CD3 on T cells, leading to potent immune activation and durable responses in relapsed/refractory multiple myeloma. Although many immune-mediated complications have been described with teclistamab, granulomatous inflammation or sarcoidosis has not been associated. We present a patient with relapsed/refractory multiple myeloma receiving teclistamab who developed new hypermetabolic lymphadenopathy on positron emission tomography/computed tomography six months after therapy initiation. The patient was asymptomatic with normal pulmonary function, borderline-elevated angiotensin-converting enzyme (ACE) levels, and mild hypercalcemia. Lymph node biopsy revealed nonnecrotizing granulomas without evidence of myeloma or infection. Extensive evaluation excluded fungal, mycobacterial, and opportunistic pathogens. Given clinical stability and sustained myeloma remission, teclistamab was continued without corticosteroid therapy. The patient remained asymptomatic with stable radiographic findings on follow-up. This represents the first reported case of sarcoidosis developing during teclistamab therapy. Recognition of this phenomenon is essential to prevent misinterpretation as myeloma progression or infectious lymphadenitis-diagnostic pitfalls that may lead to unnecessary treatment changes. This case underscores the need for heightened pharmacovigilance, systematic reporting of granulomatous toxicities associated with BCMA-directed therapies, and future immune profiling to identify patients at risk of atypical immune-mediated adverse events.
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