This work uncovers how early-life crosstalk between commensal microbes and myeloid immune cells in the developing skin barrier is pivotal in shaping long-term tissue health and in preventing chronic inflammatory disease.

3. Loss of monocytes in early-life leads to an increased susceptibility to psoriasiform inflammation in adulthood
4. Neonatal monocytes regulate IL-1 signaling to suppress spontaneous IL-17 production from cutaneous T cells.

Significant highlights:
1. We identify that commensal microbes recruit monocytes to the neonatal skin
2. Disruption in this early-life accumulation of monocytes leads to spontaneous production of the inflammatory cytokine IL-17 from T cells later in life

Model describing how commensal microbes drive the accumulation of Monocytes to the neonatal skin. Depleting these monocytes in the neonatal window leads to an IL-1 dependent aberrant release of IL-17 from cutaneous T cells later in life. This renders mice more susceptible to psoriasiform inflammation in adulthood.

Excited, grateful, and proud to share our latest research published in Immunity. None of this would have been possible without contributions from all our co-authors, across institutions. Shoutout to @scharschmidtlab.bsky.social for her unwavering support over the years! www.cell.com/immunity/ful...

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#SkinImmunity is on our list of top read articles for 2024! Skin Barrier Immunology from early life to adulthood from #EmergingLeadersInMI Niki Ubags www.mucosalimmunology.org/article/S193...

Grateful for this fun group of scientists that joined me this year in building our new lab! Happy holidays from the Dhariwala Lab 🎄🎁🎊❄️