Impaired signaling between epidermal and dendritic epidermal T cells slows wound repair in aging

Keyes B*, Liu S*, Asare A, Naik S, LevorseJ, Nikolova M, Pasoli A and Fuchs E. Impaired signaling between epidermal and dendritic epidermal T cells slows wound repair in aging. Cell.167(5)1323-1338 Nov, 2016.

Aged skin heals wounds poorly, increasing susceptibility to infections. Restoring homeostasis after wounding requires the coordinated actions of epidermal and immune cells. Here we find that both intrinsic defects and communication with immune cells are impaired in aged keratinocytes, diminishing their efficiency in restoring the skin barrier after wounding.

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Epidermal development, growth control, and homeostasis in the face of centrosome amplification

Kulukian A, Vitre B, Holland A, Naik S, Cleveland D, Fuchs E. Epidermal development, growth control, and homeostasis in the face of centrosome amplification. Proceedings of the National Academy of Sciences. 112(46):E6311-E6320 Nov, 2015

The full extent to which centrosome amplification might directly contribute to human disease is poorly understood.  Our findings challenge the role for centrosome amplification in the initiation of skin tumorigenesis and demonstrate that certain tissues are better able to cope with its burden.

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Langerhans Cells suppress skin recruitment of CD49a+ NK cells during inflammation

Scholz F, Naik S, Sutterwala, F, and Kaplan, DH. Langerhans Cells suppress skin recruitment of CD49a+ NK cells during inflammation. Journal of Immunology 1:195(5):2335-42 Jul, 2015

These data reveal a novel function for LC in the regulation of this recently described subset of skin tropic NK cells.

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Commensal-dendritic cell interactions specifies a unique protective skin immune signature.

Naik S*, Bouladoux N*, Linehan J, Han SJ, Harrison OJ, Wilhelm C, Conlan S, Himmelfarb S, Byrd A, Deming C, Quinones M, Brenchley JM, Kong H, Tussiwand R, Murphy KM, Merad M, Segre JA and Belkaid Y. Commensal-dendritic cell interactions specifies a unique protective skin immune signature. Nature. 520(7545): 104-108 April 2015.

Here we show that defined commensals dominantly affect skin immunity and identify the cellular mediators involved in this specification.This interaction may represent an evolutionary means by which the skin immune system uses fluctuating commensal signals to calibrate barrier immunity and provide heterologous protection against invasive pathogens. These findings reveal that the skin immune landscape is a highly dynamic environment that can be rapidly and specifically remodelled by encounters with defined commensals, findings that have profound implications for our understanding of tissue-specific immunity and pathologies.

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Commensal bacteria control cancer response to therapy by modulating the tumor microenvironment.

Iida N, Dzutsev A, Stewart A, Bouladoux N, Smith L, Salcedo R, Cardone M, Back T, Kiu H, Cramer S, Naik S, Patri A, Wang E, Marincola FM, Belkaid Y, Trinchieri G and Goldszmid RS. Commensal bacteria control cancer response to therapy by modulating the tumor microenvironment. Science. 342(6161):967-70. Nov, 2013

The gut microbiota influences both local and systemic inflammation. Inflammation contributes to development, progression, and treatment of cancer, but it remains unclear whether commensal bacteria affect inflammation in the sterile tumor microenvironment. Here, we show that disruption of the microbiota impairs the response of subcutaneous tumors to CpG-oligonucleotide immunotherapy and platinum chemotherapy.

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