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Video abstracts

In this video collection, authors of findings published in JCI Insight present personally guided tours of their results. The journal accepts video submissions from authors of recently accepted manuscripts. Instructions can be found on the Video Abstracts Guidelines page.

MacSpectrum platform decodes macrophage heterogeneity

In this episode, Beiyan Zhou, Chuan Li, and colleagues describe the development and application of single-cell transcriptomics-based MacSpectrum, which enables fine-mapping of monocyte/macrophage heterogeneity in healthy and disease states.


Long-term trial supports CD19-targeted CAR T cells for relapsed/refractory CLL

In this episode, Mark Geyer and colleagues demonstrate that second-generation CD19-targeted CAR T cell therapy following conditioning chemotherapy is tolerated and can produce complete remission in a subset of relapsed/refractory CLL patients.


Ovarian cancer microenvironment promotes suppressor functions in mature neutrophils

In this episode, Kelly Singel and colleagues reveal that mature neutrophils acquire a suppressive phenotype in the ovarian cancer microenvironment that is linked to complement C3 activation.


Complement receptor C3aR1-mediated protection in spinal cord injury

In this episode, Marc Ruitenberg and colleagues demonstrate that complement receptor C3aR stimulates PTEN to inhibit neutrophil-mediated inflammatory pathology following traumatic spinal cord injury.


Extreme immune decline in ART-treated HIV-infected individuals

Antiretroviral therapy (ART) is the standard of care for patients with HIV. For most patients, ART-mediate suppression of HIV replication is accompanied by reconstitution of CD4+ T cells; however, in some cases, the CD4+ T cell population is not fully restored, and these immunological nonresponders (INRs) have increased mortality. In this episode, Irini Sereti, Andrea Lisco, and colleagues identify and characterize immune parameters of 5 patients with a dramatic decline of CD4+ T cells despite ART-mediated viral suppression that is greater than that of subjects with INR. The authors define this condition as extreme immune decline (EXID) and show that it can result from the development of anti–CD4+ T cell autoantibodies and aberrant inflammasome/caspase-1 activation.

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