T cell infiltration into the brain triggers pulmonary dysfunction in murine Cryptococcus-associated IRIS

Tasuku Kawano, Jinyan Zhou, Shehata Anwar, Haneen Salah, Andrea H. Dayal, Yuzuki Ishikawa, Katelyn Boetel, Tomoko Takahashi, Kamal Sharma and Makoto Inoue ()
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Tasuku Kawano: The University of Illinois at Urbana-Champaign
Jinyan Zhou: The University of Illinois at Urbana-Champaign
Shehata Anwar: The University of Illinois at Urbana-Champaign
Haneen Salah: The University of Illinois at Urbana-Champaign
Andrea H. Dayal: The University of Illinois at Urbana-Champaign
Yuzuki Ishikawa: The University of Illinois at Urbana-Champaign
Katelyn Boetel: The University of Illinois at Urbana-Champaign
Tomoko Takahashi: Tohoku Medical and Pharmaceutical University
Kamal Sharma: University of Illinois, Chicago
Makoto Inoue: The University of Illinois at Urbana-Champaign

Nature Communications, 2023, vol. 14, issue 1, 1-15

Abstract: Abstract Cryptococcus-associated immune reconstitution inflammatory syndrome (C-IRIS) is a condition frequently occurring in immunocompromised patients receiving antiretroviral therapy. C-IRIS patients exhibit many critical symptoms, including pulmonary distress, potentially complicating the progression and recovery from this condition. Here, utilizing our previously established mouse model of unmasking C-IRIS (CnH99 preinfection and adoptive transfer of CD4+ T cells), we demonstrated that pulmonary dysfunction associated with the C-IRIS condition in mice could be attributed to the infiltration of CD4+ T cells into the brain via the CCL8-CCR5 axis, which triggers the nucleus tractus solitarius (NTS) neuronal damage and neuronal disconnection via upregulated ephrin B3 and semaphorin 6B in CD4+ T cells. Our findings provide unique insight into the mechanism behind pulmonary dysfunction in C-IRIS and nominate potential therapeutic targets for treatment.

Date: 2023
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DOI: 10.1038/s41467-023-39518-x

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