scholarly journals A Quantitative Multivariate Model of Human Dendritic Cell-T Helper Cell Communication

Cell ◽  
2019 ◽  
Vol 179 (2) ◽  
pp. 432-447.e21 ◽  
Author(s):  
Maximilien Grandclaudon ◽  
Marie Perrot-Dockès ◽  
Coline Trichot ◽  
Léa Karpf ◽  
Omar Abouzid ◽  
...  
Author(s):  
Maximilien Grandclaudon ◽  
Marie Perrot-Dockès ◽  
Coline Trichot ◽  
Omar Mostafa-Abouzid ◽  
Wassim Abou-Jaoudé ◽  
...  

2007 ◽  
Vol 178 (3) ◽  
pp. 1468-1476 ◽  
Author(s):  
Elke Scandella ◽  
Katja Fink ◽  
Tobias Junt ◽  
Beatrice M. Senn ◽  
Evelyn Lattmann ◽  
...  

Immunity ◽  
2015 ◽  
Vol 42 (2) ◽  
pp. 356-366 ◽  
Author(s):  
Sakeen W. Kashem ◽  
Botond Z. Igyártó ◽  
Maryam Gerami-Nejad ◽  
Yosuke Kumamoto ◽  
Javed Mohammed ◽  
...  

1995 ◽  
Vol 73 (6) ◽  
pp. 537-543 ◽  
Author(s):  
MARGARET A BAIRD ◽  
DEREK NJ HART ◽  
NEVIN ABERNETHY ◽  
JAMES D WATSON

Immunity ◽  
2011 ◽  
Vol 35 (2) ◽  
pp. 260-272 ◽  
Author(s):  
Botond Z. Igyártó ◽  
Krystal Haley ◽  
Daniela Ortner ◽  
Aleh Bobr ◽  
Maryam Gerami-Nejad ◽  
...  

Blood ◽  
2010 ◽  
Vol 116 (16) ◽  
pp. 2942-2949 ◽  
Author(s):  
Karel Otero ◽  
Annunciata Vecchi ◽  
Emilio Hirsch ◽  
Jennifer Kearley ◽  
William Vermi ◽  
...  

Abstract Chemokine CC motif receptor-like 2 (CCRL2) is a heptahelic transmembrane receptor that shows the highest degree of homology with CCR1, an inflammatory chemokine receptor. CCRL2 mRNA was rapidly (30 minutes) and transiently (2-4 hours) regulated during dendritic cell (DC) maturation. Protein expression paralleled RNA regulation. In vivo, CCRL2 was expressed by activated DC and macrophages, but not by eosinophils and T cells. CCRL2−/− mice showed normal recruitment of circulating DC into the lung, but a defective trafficking of antigen-loaded lung DC to mediastinal lymph nodes. This defect was associated to a reduction in lymph node cellularity and reduced priming of T helper cell 2 response. CCRL2−/− mice were protected in a model of ovalbumin-induced airway inflammation, with reduced leukocyte recruitment in the BAL (eosinophils and mononuclear cells) and reduced production of the T helper cell 2 cytokines, interleukin-4 and -5, and chemokines CCL11 and CCL17. The central role of CCRL2 deficiency in DC was supported by the fact that adoptive transfer of CCRL2−/− antigen-loaded DC in wild-type animals recapitulated the phenotype observed in knockout mice. These data show a nonredundant role of CCRL2 in lung DC trafficking and propose a role for this receptor in the control of excessive airway inflammatory responses.


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