Literature DB >> 30504420

CD62L Is a Functional and Phenotypic Marker for Circulating Innate Lymphoid Cell Precursors.

Yotam E Bar-Ephraim1, Jasper J Koning1, Estefany Burniol Ruiz1, Tanja Konijn1, Vera P Mourits1, Kim A Lakeman1, Louis Boon2, Marijn Bögels1, J Peter van Maanen3, Joke M M Den Haan1, Marjolein van Egmond1, Gerd Bouma4, Rogier M Reijmers1, Reina E Mebius5.   

Abstract

Innate lymphoid cells (ILCs) guard epithelial tissue integrity during homeostasis, but can be potent immune effector cells during inflammation. Precursors to all ILC subsets (ILC precursors [ILCP]) have been identified in human peripheral blood (PB). We found that during homeostasis, ILCP in PB of mouse and human expressed homing receptors for secondary lymphoid organs, mainly CD62L. These ILCP entered mouse lymph nodes in a CD62L-dependent way and relied on S1P receptors for their exit. Importantly, CD62L expression was absent on human ILCs expressing NKp44 in tonsils and PB of Crohn disease patients, and relatively fewer CD62L+ ILCP were present in PB of Crohn disease patients. These data are in agreement with selective expression of CD62L on nonactivated ILCP. As such, we conclude that CD62L not only serves as a functional marker of ILCP, but has potential to be used in the clinic as a diagnostic marker in inflammatory disorders.
Copyright © 2018 by The American Association of Immunologists, Inc.

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Year:  2018        PMID: 30504420     DOI: 10.4049/jimmunol.1701153

Source DB:  PubMed          Journal:  J Immunol        ISSN: 0022-1767            Impact factor:   5.422


  16 in total

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4.  The Prostaglandin D2 Receptor CRTH2 Promotes IL-33-Induced ILC2 Accumulation in the Lung.

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6.  Crohn's Disease Is Associated With Activation of Circulating Innate Lymphoid Cells.

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7.  KLRG1 and NKp46 discriminate subpopulations of human CD117+CRTH2- ILCs biased toward ILC2 or ILC3.

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Review 9.  Metabolic Control of Innate Lymphoid Cell Migration.

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10.  Reduction of circulating innate lymphoid cell progenitors results in impaired cytokine production by innate lymphoid cells in patients with lupus nephritis.

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