Migratory dermal γδ T cells determine the balance between lung immunity and tissue damage duringNippostrongylus brasiliensisinfection

Many helminth parasites migrate through multiple host organs during infection but how immunity is regulated across
these tissues is still poorly understood. To investigate the cellular and molecular aspects of inter-tissue communication during infection we established a percutaneous infection model
with the tissue-migrating nematode Nippostrongylus brasiliensis. High-dimension profiling of the initial cutaneous immune
response revealed that dermal γδ T cells become activated, engage cell motility-associated transcriptional pathways and leave
the skin after parasite invasion. Chemical and genetic inhibition of leukocyte migration prevents the accumulation of IL-17-
producing γδ T cells in the lungs. Notably, bypassing the skin
phase of infection, and therefore preventing dermal γδ T cell migration, dampens the increase in early IL-17 production in the
lungs, and, instead, leads to enhanced IFNγ responses together
with increased lung damage. Collectively, our data highlights a
critical skin–lung axis regulating host-parasite interactions and
safeguarding lung health