WordNet

showing care; "a protective mother"
(usually followed by `of'
intended or adapted to afford protection of some kind; "a protective covering"; "the use of protective masks and equipment"; "protective coatings"; "kept the drunken sailor in protective custody"; "animals with protective coloring"; "protective tariffs"
(medicine) the condition in which an organism can resist disease (同)resistance
the quality of being unaffected by something; "immunity to criticism"

PrepTutorEJDIC

保護の,保護する;(…を)保護する《+『toward』+『名』》
〈U〉(病気に対する)免疫《+『from』(『to, against』)+『名』》 / (義務・税などの)免除《+『from』(『to, against』)+『名』》

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1. 結核の免疫学 immunology of tuberculosis
2. 予防接種に対する免疫応答の評価 assessing the immunologic response to vaccination
3. 新生児の免疫 immunity of the newborn
4. 胎児および新生児における免疫細胞の発達 the development of immune cells in the fetus and neonate
5. HIV-1感染の免疫学 immunology of hiv 1 infection

English Journal

Activation of B cells by a dendritic cell-targeted oral vaccine.

Sahay B, Owen JL, Yang T, Zadeh M, Lightfoot YL, Ge JW, Mohamadzadeh M1.Author information 1Department of Infectious Diseases & Pathology, Division of Gastroenterology, Hepatology & Nutrition, Department of Medicine, University of Florida, 2015 SW16th Ave, Building 1017, Room: V3-149, Gainesville, FL 32608, USA. m.zadeh@ufl.edu.AbstractProduction of long-lived, high affinity humoral immunity is an essential characteristic of successful vaccination and requires cognate interactions between T and B cells in germinal centers. Within germinal centers, specialized T follicular helper cells assist B cells and regulate the antibody response by mediating the differentiation of B cells into memory or plasma cells after exposure to T cell-dependent antigens. It is now appreciated that local immune responses are also essential for protection against infectious diseases that gain entry to the host by the mucosal route; therefore, targeting the mucosal compartments is the optimum strategy to induce protective immunity. However, because the gastrointestinal mucosae are exposed to large amounts of environmental and dietary antigens on a daily basis, immune regulatory mechanisms exist to favor tolerance and discourage autoimmunity at these sites. Thus, mucosal vaccination strategies must ensure that the immunogen is efficiently taken up by the antigen presenting cells, and that the vaccine is capable of activating humoral and cellular immunity, while avoiding the induction of tolerance. Despite significant progress in mucosal vaccination, this potent platform for immunotherapy and disease prevention must be further explored and refined. Here we discuss recent progress in the understanding of the role of different phenotypes of B cells in the development of an efficacious mucosal vaccine against infectious disease.
Current pharmaceutical biotechnology.Curr Pharm Biotechnol.2014 Nov;14(10):867-77.
Production of long-lived, high affinity humoral immunity is an essential characteristic of successful vaccination and requires cognate interactions between T and B cells in germinal centers. Within germinal centers, specialized T follicular helper cells assist B cells and regulate the antibody respo
PMID 24372255

The C-type lectin-like domain containing proteins Clec-39 and Clec-49 are crucial for Caenorhabditis elegans immunity against Serratia marcescens infection.

Miltsch SM1, Seeberger PH2, Lepenies B3.Author information 1Max Planck Institute of Colloids and Interfaces, Department of Biomolecular Systems, Am Mühlenberg 1, 14476 Potsdam, Germany.2Max Planck Institute of Colloids and Interfaces, Department of Biomolecular Systems, Am Mühlenberg 1, 14476 Potsdam, Germany; Freie Universität Berlin, Institute of Chemistry and Biochemistry, Arnimallee 22, 14195 Berlin, Germany.3Max Planck Institute of Colloids and Interfaces, Department of Biomolecular Systems, Am Mühlenberg 1, 14476 Potsdam, Germany; Freie Universität Berlin, Institute of Chemistry and Biochemistry, Arnimallee 22, 14195 Berlin, Germany. Electronic address: Bernd.Lepenies@mpikg.mpg.de.AbstractCaenorhabditis elegans exhibits protective immunity against a variety of fungal and bacterial pathogens. Since C. elegans lacks an adaptive immune system, pathogen recognition is mediated entirely by innate immunity. To date, little is known about the involvement of pattern recognition receptors (PRRs) in pathogen sensing as part of the C. elegans immunity. C-type lectin-like domain (CTLD) containing proteins represent a superfamily of PRRs. A large number of genes encoding for CTLD proteins are present in the C. elegans genome, however the role of CTLD proteins in bacterial recognition and antibacterial immunity has not yet been determined. In this study, we investigated the function of selected C. elegans CTLD proteins during infection with the Gram-negative bacterium Serratia marcescens. Wild-type and CTLD gene-deficient C. elegans strains were compared in their susceptibility to S. marcescens infection. Interestingly, survival and egg laying were significantly reduced in strains deficient for clec-39 and clec-49 indicating a role for both CTLD proteins in C. elegans immune defense against bacteria as evidenced by using S. marcescens infection. Binding studies with recombinantly expressed Clec-39-Fc and Clec-49-Fc fusion proteins revealed that both CTLD proteins recognized live bacteria in a Ca(2+)-independent manner. This study provides insight into the role of CTLD proteins in C. elegans immunity and demonstrates their function during bacterial infection.
Developmental and comparative immunology.Dev Comp Immunol.2014 Jul;45(1):67-73. doi: 10.1016/j.dci.2014.02.002. Epub 2014 Feb 15.
Caenorhabditis elegans exhibits protective immunity against a variety of fungal and bacterial pathogens. Since C. elegans lacks an adaptive immune system, pathogen recognition is mediated entirely by innate immunity. To date, little is known about the involvement of pattern recognition receptors (PR
PMID 24534554

Innate immune responses of airway epithelial cells to infection with Equine herpesvirus-1.

Soboll Hussey G1, Ashton LV2, Quintana AM2, Lunn DP3, Goehring LS4, Annis K2, Landolt G2.Author information 1Department of Pathobiology and Diagnostic Investigation, College of Veterinary Medicine, Veterinary Medical Center, Room A13, 784 Wilson Road, East Lansing, MI 48824, USA. Electronic address: husseygi@msu.edu.2Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, 300 W. Drake Road, Fort Collins, CO 80523, USA.3North Carolina State University, 1060 William Moore Drive, Raleigh, NC 276074, USA.4Faculty of Veterinary Medicine, Ludwig-Maximilians University, Munich, Germany.AbstractEquine herpesvirus-1 (EHV-1) is the cause of respiratory disease, abortion and myelitis in horses worldwide. Protection following infection or vaccination is typically incomplete and this lack of protective immunity is thought to be due to the immunomodulatory properties of EHV-1. EHV-1 immune modulation is likely initiated early in the infection cycle at the respiratory epithelium, but to date, immunity to EHV-1 at the epithelial cell barrier remains poorly characterized. Thus, the purpose of this study was to use a recently established primary equine respiratory epithelial cell culture (EREC) system to characterize innate immunity to EHV-1. Differentiated ERECs were inoculated with a neuropathogenic strain of EHV-1 and cytokine responses were determined using quantitative real-time polymerase chain reaction and ELISA. Major histocompatibility complex (MHC)-I and MHC-II as well as toll-like receptor (TLR)3 and TLR9 protein expression were examined using fluorescence activated cell-sorting analysis and chemotaxis of neutrophils and monocytes were evaluated using chemotaxis assays. Infection with EHV-1 resulted in increased expression of TLR3 and 9 as well as inflammatory cytokines (IL-1, TNF-alpha, IFN-alpha, and IL-6) and chemokines (IL-8, MCP-1). In contrast, EHV-1 infection caused marked decreases of MHC-I and MHC-II expression as well as a reduction in IFN-gamma production. In summary, these results provide an initial characterization of the early immune response to EHV-1 at the epithelial cell barrier and show that, while EHV-1 maintains induction of an inflammatory response, it causes an attenuation of IFN-gamma responses and down-modulates expression of MHC-I and MHC-II, which are important molecules for antigen presentation.
Veterinary microbiology.Vet Microbiol.2014 May 14;170(1-2):28-38. doi: 10.1016/j.vetmic.2014.01.018. Epub 2014 Feb 3.
Equine herpesvirus-1 (EHV-1) is the cause of respiratory disease, abortion and myelitis in horses worldwide. Protection following infection or vaccination is typically incomplete and this lack of protective immunity is thought to be due to the immunomodulatory properties of EHV-1. EHV-1 immune modul
PMID 24560592