NDLI: The Tat-conjugated N-terminal region of mucin antigen 1 (MUC1) induces protective immunity against MUC1-expressing tumours.

Please wait, while we are loading the content...

A novel population of human CD56+ human leucocyte antigen D-related (HLA-DR+) colonic lamina propria cells is associated with inflammation in ulcerative colitis.

Increased frequencies of T helper type 17 cells in the peripheral blood of patients with acute myeloid leukaemia.

Mechanisms and clinical implications of glucocorticosteroids in the treatment of allergic rhinitis.

Reduced incidence and severity of experimental autoimmune arthritis in mice expressing catalytically inactive A disintegrin and metalloproteinase 8 (ADAM8).

Increased levels of T cell granzyme b in bronchiolitis obliterans syndrome are not suppressed adequately by current immunosuppressive regimens.

BAFF: a local and systemic target in autoimmune diseases

Chronic antigenic stimuli as a possible explanation for the immunodepression caused by liver cirrhosis.

Prolonging microtubule dysruption enhances the immunogenicity of chronic lymphocytic leukaemia cells.

The Tat-conjugated N-terminal region of mucin antigen 1 (MUC1) induces protective immunity against MUC1-expressing tumours.

Chemokines and common variable immunodeficiency; possible contribution of CCL19, CCL21 and CCR7 to immune dysregulation.

Year: 2009 Volume: 158 Issue: 1

Year: 2009 Volume: 158 Issue: Supplementary 1

Year: 2009 Volume: 157

Year: 2009 Volume: 156

Year: 2009 Volume: 155

Year: 2008 Volume: 154

Year: 2008 Volume: 153

Year: 2008 Volume: 152

Year: 2008 Volume: 151

Year: 2007 Volume: 150

The Tat-conjugated N-terminal region of mucin antigen 1 (MUC1) induces protective immunity against MUC1-expressing tumours.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Yang, H. Cho, N-H Seong, S-Y
Description	Author Affiliation: Yang H ( Department of Microbiology and Immunology, Seoul National University College of Medicine, Seoul, Korea.)
Abstract	Mucin antigen 1 (MUC1) is overexpressed on various human adenocarcinomas and haematological malignancies and has long been used as a target antigen for cancer immunotherapy. Most of the preclinical and clinical studies using MUC1 have used the tandem repeat region of MUC1, which could be presented by only a limited set of major histocompatibility complex haplotypes. Here, we evaluated N-terminal region (2-147 amino acids) of MUC1 (MUC1-N) for dendritic cell (DC)-based cancer immunotherapy. We used Esherichia coli-derived MUC1-N that was fused to the protein transduction domain of human immunodeficiency virus Tat protein for three reasons. First, mature DCs do not phagocytose soluble protein antigens. Secondly, tumour cells express underglycosylated MUC1, which can generate epitopes repertoire that differs from normal cells, which express hyperglycosylated MUC1. Finally, aberrantly glycosylated MUC1 has been known to impair DC function. In our study, Tat-MUC1-N-loaded DCs induced type 1 T cell responses as well as cytotoxic T lymphocytes efficiently. Furthermore, they could break tolerance in the transgenic breast tumour mouse model, where MUC1-positive breast cancers grow spontaneously. Compared with DCs pulsed with unconjugated MUC1-N, DCs loaded with Tat-conjugated MUC1-N could delay tumour growth more effectively in the transgenic tumour model as well as in the tumour injection model. These results suggest that the recombinant N-terminal part of MUC1, which may provide a diverse epitope repertoire, could be utilized as an effective tumour antigen for DC-based cancer immunotherapy.
File Format	HTM / HTML
ISSN	00099104
e-ISSN	13652249
DOI	10.1111/j.1365-2249.2009.03997.x
Journal	Clinical & Experimental Immunology
Issue Number	2
Volume Number	158
Language	English
Publisher	Wiley-Blackwell
Publisher Date	2009-11-01
Publisher Place	Great Britain (UK)
Access Restriction	Open
Subject Keyword	Discipline Immunology Cancer Vaccines Immunology Mammary Neoplasms, Experimental Prevention & Control Mucin-1 Metabolism Neoplasm Proteins Tat Gene Products, Human Immunodeficiency Virus Animals Cell Differentiation Cell Line, Tumor Cell Proliferation Cytokines Biosynthesis Cytotoxicity, Immunologic Dendritic Cells Transplantation Lymphocyte Activation Pathology Mice Mice, Inbred C57bl Mice, Transgenic Recombinant Proteins Spleen Survival Analysis Transduction, Genetic Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

The Tat-conjugated N-terminal region of mucin antigen 1 (MUC1) induces protective immunity against MUC1-expressing tumours

Immune recognition of tumor-associated mucin MUC1 is achieved by a fully synthetic aberrantly glycosylated MUC1 tripartite vaccine.

Protective anti-tumour immune responses by murine dendritic cells pulsed with recombinant Tat-carcinoembryonic antigen derived from Escherichia coli.

Targeting antigen to mouse dendritic cells via Clec9A induces potent CD4 T cell responses biased toward a follicular helper phenotype.

Vaccination with TAT-antigen fusion protein induces protective, CD8(+) T cell-mediated immunity against Leishmania major.

Fully Synthetic Self-Adjuvanting Thioether-Conjugated GlycopeptideLipopeptide Antitumor Vaccines for the Induction of Complement-Dependent Cytotoxicity against Tumor Cells

Leukocyte-associated Ig-like receptor-1-deficient mice have an altered immune cell phenotype.

Dendritic cells require STAT-1 phosphorylated at its transactivating domain for the induction of peptide-specific CTL.

MUC1 expressing tumor growth was retarded after human mucin 1 (MUC1) plasmid DNA immunization

The Tat-conjugated N-terminal region of mucin antigen 1 (MUC1) induces protective immunity against MUC1-expressing tumours.

Similar Documents

The Tat-conjugated N-terminal region of mucin antigen 1 (MUC1) induces protective immunity against MUC1-expressing tumours

Immune recognition of tumor-associated mucin MUC1 is achieved by a fully synthetic aberrantly glycosylated MUC1 tripartite vaccine.

Protective anti-tumour immune responses by murine dendritic cells pulsed with recombinant Tat-carcinoembryonic antigen derived from Escherichia coli.

Targeting antigen to mouse dendritic cells via Clec9A induces potent CD4 T cell responses biased toward a follicular helper phenotype.

Vaccination with TAT-antigen fusion protein induces protective, CD8(+) T cell-mediated immunity against Leishmania major.

Fully Synthetic Self-Adjuvanting Thioether-Conjugated GlycopeptideLipopeptide Antitumor Vaccines for the Induction of Complement-Dependent Cytotoxicity against Tumor Cells

Leukocyte-associated Ig-like receptor-1-deficient mice have an altered immune cell phenotype.

Dendritic cells require STAT-1 phosphorylated at its transactivating domain for the induction of peptide-specific CTL.

MUC1 expressing tumor growth was retarded after human mucin 1 (MUC1) plasmid DNA immunization

The Tat-conjugated N-terminal region of mucin antigen 1 (MUC1) induces protective immunity against MUC1-expressing tumours.