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Barber, Daniel L; Sakai, Shunsuke; Kudchadkar, Ragini R; Fling, Steven P; Day, Tracey A; Vergara, Julie A; Ashkin, David; Cheng, Jonathan H; Lundgren, Lisa M; Raabe, Vanessa N; Kraft, Colleen S; Nieva, Jorge J; Cheever, Martin A; Nghiem, Paul T; Sharon, Elad
Science translational medicine, 01/2019, Volume: 11, Issue: 475Journal Article
Because of the well-established therapeutic benefit of boosting antitumor responses through blockade of the T cell inhibitory receptor PD-1, it has been proposed that PD-1 blockade could also be useful in infectious disease settings, including (Mtb) infection. However, in preclinical models, Mtb-infected PD-1 mice mount exaggerated T 1 responses that drive lethal immunopathology. Multiple cases of tuberculosis during PD-1 blockade have been observed in patients with cancer, but in humans little is understood about Mtb-specific immune responses during checkpoint blockade-associated tuberculosis. Here, we report two more cases. We describe a patient who succumbed to disseminated tuberculosis after PD-1 blockade for treatment of nasopharyngeal carcinoma, and we examine Mtb-specific immune responses in a patient with Merkel cell carcinoma who developed checkpoint blockade-associated tuberculosis and was successfully treated for the infection. After anti-PD-1 administration, interferon-γ-producing Mtb-specific CD4 T cells became more prevalent in the blood, and a tuberculoma developed a few months thereafter. Mtb-specific T 17 cells, CD8 T cells, regulatory T cells, and antibody abundance did not change before the appearance of the granuloma. These results are consistent with the murine model data and suggest that boosting T 1 function with PD-1 blockade may increase the risk or severity of tuberculosis in humans.
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