Peripheral CD103+ dendritic cells form a unified subset developmentally related to CD8α+ conventional dendritic cells

Autor: Sun-Sang J. Sung, Masako Kohyama, Wumesh Kc, Loralyn A. Benoit, Wataru Ise, Theresa L. Murphy, Thaddeus S. Stappenbeck, Kai Hildner, Drew G. Michael, Paul A. Klekotka, Michael J. Holtzman, Brian T. Edelson, Clara Moon, Richard Juang, Deepta Bhattacharya, Kenneth M. Murphy, Jörn C. Albring
Rok vydání: 2010
Předmět:
Male
T-Lymphocytes
Gene Expression
Priming (immunology)
Dermatitis
Contact
Sendai virus
Mice
Intestinal mucosa
Immunology and Allergy
Cytotoxic T cell
Mesenteric lymph nodes
Mesentery
Intestinal Mucosa
Lung
Oligonucleotide Array Sequence Analysis
Skin
Mice
Knockout
Mice
Inbred C3H
education.field_of_study
hemic and immune systems
Basic-Leucine Zipper Transcription Factors
medicine.anatomical_structure
Antigens
Surface
Interferon Regulatory Factors
Female
medicine.symptom
Integrin alpha Chains
CD8 Antigens
Immunology
Population
Receptor
Macrophage Colony-Stimulating Factor
chemical and pharmacologic phenomena
Inflammation
Biology
Respirovirus Infections
Article
Antigens
CD
medicine
Animals
education
Dendritic Cells
Mice
Mutant Strains
Mice
Inbred C57BL
Repressor Proteins
fms-Like Tyrosine Kinase 3
Fms-Like Tyrosine Kinase 3
Dinitrofluorobenzene
Lymph Nodes
IRF8
Transcription Factors
Zdroj: The Journal of Experimental Medicine
ISSN: 1540-9538
0022-1007
DOI: 10.1084/jem.20091627
Popis: Although CD103-expressing dendritic cells (DCs) are widely present in nonlymphoid tissues, the transcription factors controlling their development and their relationship to other DC subsets remain unclear. Mice lacking the transcription factor Batf3 have a defect in the development of CD8alpha+ conventional DCs (cDCs) within lymphoid tissues. We demonstrate that Batf3(-/-) mice also lack CD103+CD11b- DCs in the lung, intestine, mesenteric lymph nodes (MLNs), dermis, and skin-draining lymph nodes. Notably, Batf3(-/-) mice displayed reduced priming of CD8 T cells after pulmonary Sendai virus infection, with increased pulmonary inflammation. In the MLNs and intestine, Batf3 deficiency resulted in the specific lack of CD103+CD11b- DCs, with the population of CD103+CD11b+ DCs remaining intact. Batf3(-/-) mice showed no evidence of spontaneous gastrointestinal inflammation and had a normal contact hypersensitivity (CHS) response, despite previous suggestions that CD103+ DCs were required for immune homeostasis in the gut and CHS. The relationship between CD8alpha+ cDCs and nonlymphoid CD103+ DCs implied by their shared dependence on Batf3 was further supported by similar patterns of gene expression and their shared developmental dependence on the transcription factor Irf8. These data provide evidence for a developmental relationship between lymphoid organ-resident CD8alpha+ cDCs and nonlymphoid CD103+ DCs.
Databáze: OpenAIRE
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