Dendritic Cells Recruitment and In Vivo Priming of CD8+ CTL Induced by a Single Topical or Transepithelial Immunization Via the Buccal Mucosa with Measles Virus Nucleoprotein

Etchart, Nathalie; Desmoulins, Pierre-Olivier; Chemin, Karine; Maliszewski, Charles R.; Dubois, Bertrand; Wild, Fabian; Kaiserlian, Dominique

doi:10.4049/jimmunol.167.1.384

Cited by 37 publications

(35 citation statements)

References 54 publications

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“…Similar to their equivalents in the epidermis, oral LCs residing in the epithelium express langerin and EpCAM and contain Birbeck granules (Arizon et al, 2012;Kotani et al, 1991;Newcomb and Powell, 1986). Furthermore, several studies have demonstrated a high similarity between the structure and function of the buccal and skin immune systems (Barrett et al, 1993;Etchart et al, 2001;Le Borgne et al, 2006). In addition to the buccal mucosa, the keratinized gingival mucosa represents another important tissue for the study of LCs.…”

Section: Introductionmentioning

confidence: 96%

Distinct Murine Mucosal Langerhans Cell Subsets Develop from Pre-dendritic Cells and Monocytes

et al. 2015

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Langerhans cells (LCs) populate the mucosal epithelium, a major entry portal for pathogens, yet their ontogeny remains unclear. We found that, in contrast to skin LCs originating from self-renewing radioresistant embryonic precursors, oral mucosal LCs derive from circulating radiosensitive precursors. Mucosal LCs can be segregated into CD103(+)CD11b(lo) (CD103(+)) and CD11b(+)CD103(-) (CD11b(+)) subsets. We further demonstrated that similar to non-lymphoid dendritic cells (DCs), CD103(+) LCs originate from pre-DCs, whereas CD11b(+) LCs differentiate from both pre-DCs and monocytic precursors. Despite this ontogenetic discrepancy between skin and mucosal LCs, the transcriptomic signature and immunological function of oral LCs highly resemble those of skin LCs but not DCs. These findings, along with the epithelial position, morphology, and expression of the LC-associated phenotype strongly suggest that oral mucosal LCs are genuine LCs. Collectively, in a tissue-dependent manner, murine LCs differentiate from at least three distinct precursors (embryonic, pre-DC, and monocytic) in steady state.

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Section: Introductionmentioning

confidence: 96%

Distinct Murine Mucosal Langerhans Cell Subsets Develop from Pre-dendritic Cells and Monocytes

et al. 2015

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“…Moreover, efficient helper CD4 ϩ -T and cytotoxic CD8 ϩ -T-cell responses against N are generated during the course of MV infection (23,24,59). MV-N induces, in the absence of other viral proteins, N-specific T-cell responses, a systemic anti-N antibody response, and protection against MV infection (12,39). Thus, MV infection is associated with an effective Nspecific response that leads, with other events, to viral clearance, recovery from disease in 2 weeks, and to a protective immune response against reinfection.…”

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confidence: 99%

Measles Virus (MV) Nucleoprotein Binds to a Novel Cell Surface Receptor Distinct from FcγRII via Its C-Terminal Domain: Role in MV-Induced Immunosuppression

Laine

Trescol-Biémont

Longhi

et al. 2003

J Virol

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“…It has been demonstrated that buccal application of recombinant N with- (11). Thus, immunosuppression during measles is accompanied by a strong anti-measles immune response, particularly against N, presenting an "immunological paradox" (20,22).…”

Section: Discussionmentioning

confidence: 99%

Cell Surface Delivery of the Measles Virus Nucleoprotein: a Viral Strategy To Induce Immunosuppression

Marie

Saltel

Escola

et al. 2004

J Virol

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Although only a few blood cells are infected during measles, this infectious disease is followed by acute immunosuppression, associated with high infant mortality. Measles virus nucleoprotein has been suggested to contribute to virus-induced inhibition of the immune response. However, it has been difficult to understand how this cytosolic viral protein could leave an infected cell and then perturb the immune response. Here we demonstrate that intracellularly synthesized nucleoprotein enters the late endocytic compartment, where it recruits its cellular ligand, the Fc␥ receptor. Nucleoprotein is then expressed at the surfaces of infected leukocytes associated with the Fc␥ receptor and is secreted into the extracellular compartment, allowing its interaction with uninfected cells. Finally, cell-derived nucleoprotein inhibits the secretion of interleukin-12 and the generation of the inflammatory reaction, both shown to be impaired during measles. These results reveal nucleoprotein egress from infected cells as a novel strategy in measles-induced immunosuppression.Measles virus (MV) is among the most contagious pathogens for humans, still infecting more than 40 million people and causing the death of around 1 million a year (33). MV is responsible for an acute childhood disease which is widespread in developing countries, with sporadic outbreaks in industrialized countries despite vaccination. MV is a morbillivirus with a single-stranded, negative-sense RNA genome, encoding six structural proteins. The lipid bilayer contains two envelope glycoproteins, the hemagglutinin (H) and the fusion protein (F). The matrix protein (M) supplies an interface between the envelope and the virion core, composed of viral RNA, the nucleocapsid protein (N), the phosphoprotein (P), and the large protein (L). The function of the N protein appears to be packaging and protection of the viral genomic nucleic acid and formation of a replication complex, along with the P and L proteins (20). N is the most abundant of the viral proteins, synthesized on free ribosomes and folded in the cytoplasm, where it binds viral RNA and forms intracellular inclusions (17). This 60-kDa protein has the capacity to self-assemble into nucleocapsids on cellular RNA as well, in the absence of any of the other MV gene products (43). MV infection is initiated by the attachment of the virus via MV H to one of its specific receptors, CD46 or CD150, followed by virus-cell fusion and release of the nucleocapsid into the cytoplasm (20,46).MV causes a profound suppression of the immune system that permits opportunistic infections, leading to high infant morbidity and mortality. The immune abnormalities that are most evident are in the cellular arm of the immune response and include disappearance of the delayed-type hypersensitivity responses (45, 49), impaired proliferation of peripheral blood lymphocytes (PBLs) (23), and allospecific cytotoxicity (15). Type 2 polarization of cytokine responses occurs during late stages of measles: the production of interleukin 4 (IL-4)...

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Dendritic Cells Recruitment and In Vivo Priming of CD8+ CTL Induced by a Single Topical or Transepithelial Immunization Via the Buccal Mucosa with Measles Virus Nucleoprotein

Cited by 37 publications

References 54 publications

Distinct Murine Mucosal Langerhans Cell Subsets Develop from Pre-dendritic Cells and Monocytes

Distinct Murine Mucosal Langerhans Cell Subsets Develop from Pre-dendritic Cells and Monocytes

Measles Virus (MV) Nucleoprotein Binds to a Novel Cell Surface Receptor Distinct from FcγRII via Its C-Terminal Domain: Role in MV-Induced Immunosuppression

Cell Surface Delivery of the Measles Virus Nucleoprotein: a Viral Strategy To Induce Immunosuppression

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