Dendritic Cells and their Receptors in Antitumor Immune Response

Srivastava, Raghvendra M.; Khar, Ashok

doi:10.2174/156652409788970715

Cited by 4 publications

(2 citation statements)

References 173 publications

(210 reference statements)

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“…In addition to TA uptake and processing, T cell-based antitumor immune responses are dependent on DC receptors and maturation phenotype [29]. Along with the uptake of antigenic complexes, Fc γ R also modulate the DC maturation status, and the balance between the activating and inhibitory Fc γ R greatly influence the outcome of immunological responses.…”

Section: Ta-specific Mabs Initiate Nk:dc Cross Talk Leading To Cellulmentioning

confidence: 99%

Natural killer (NK):dendritic cell (DC) cross talk induced by therapeutic monoclonal antibody triggers tumor antigen-specific T cell immunity

et al. 2011

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Tumor antigen (TA)-targeted monoclonal antibodies (mAb), trastuzumab, cetuximab, panitumumab, and rituximab, have been among the most successful new therapies in the present generation. Clinical activity is observed as a single agent, or in combination with radiotherapy or chemotherapy, against metastatic colorectal cancer, head and neck cancer, breast cancer, and follicular lymphoma. However, the activity is seen only in a minority of patients. Thus, an intense need exists to define the mechanism of action of these immunoactive mAb. Here, we discuss some of the likely immunological events that occur in treated patients: antibody-dependent cellular cytotoxicity (ADCC), cross talk among immune cells including NK cells and dendritic cells (DCs), and generation of TA-specific T lymphocyte responses. We present evidence supporting the induction of “NK:DC cross talk,” leading to priming of TA-specific cellular immunity. These observations show that mAb-mediated NK cell activation can be greatly enhanced by the action of stimulatory cytokines and surface molecules on maturing DC and that NK:DC interaction facilitates the recruitment of both NK cells and DC to the tumor site(s). The cooperative, reciprocal stimulatory activity of both NK cells and DC can modulate both the innate immune response in the local tumor microenvironment and the adaptive immune response in secondary lymphoid organs. These events likely contribute to clinical activity, as well as provide a potential biomarker of response to mAb therapy.

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Section: Ta-specific Mabs Initiate Nk:dc Cross Talk Leading To Cellulmentioning

confidence: 99%

Natural killer (NK):dendritic cell (DC) cross talk induced by therapeutic monoclonal antibody triggers tumor antigen-specific T cell immunity

et al. 2011

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“…No causative link can be made between the increase in DC‐SIGN expression prior to increased Musashi‐1 expression, but these findings prompt us to speculate that dendritic cell‐driven immune inflammation, occurring in the connective tissue stroma of the tunica mucosa, might focally affect the microenvironment in a manner that destabilizes a dormant state of stem cells/cancer stem cells. Immune inflammation may thus contribute to tumor development in the esophagus by altering the tissue microenvironment 49,50 …”

Section: Discussionmentioning

confidence: 99%

Expression of the putative stem cell marker Musashi-1 in Barrett's esophagus and esophageal adenocarcinoma

Bobryshev¹,

Freeman²,

Botelho³

et al. 2010

Diseases of the Esophagus

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The cancer stem cell theory states that cancers contain tumor-forming cells that have the ability to self-renew as well as give rise to cells that differentiate. Cancer stem cells have been identified in several solid tumors, but stem cells in normal human esophagus or in Barrett's esophagus or adenocarcinoma have not been reported. Musashi-1 is expressed by the crypt base columnar cells identified as intestinal stem cells. In other diseases of the gastrointestinal tract, local inflammation of the tunica mucosa may be an initiating factor of alteration of focal tissue 'niches,' where dormant stem cells locate. The present study investigated whether Musashi-1 is expressed in the esophagus and its relation to immune inflammation of the mucosa in Barrett's esophagus and esophageal adenocarcinoma. A total of 41 esophageal tissue specimens from 41 patients were studied. Of these, 15 were esophageal adenocarcinoma, 17 were Barrett's esophagus (10 intestinal metaplasia and 7 dysplasia), and 9 were normal squamous esophagus tissue specimens from patients without esophageal pathology. Immunohistochemistry was performed using antibodies to Musashi-1 and to a set of cell type-specific markers. A multiplexed tandem polymerase chain reaction method was used to measure the relative mRNA expression levels of Musashi-1 and the specific dendritic cell marker dendritic cell-specific intercellular molecule-3 (ICAM-3)-grabbing nonintegrin. Immunohistochemistry demonstrated the presence of small numbers of Musashi-1+ cells scattered in the connective tissue stroma and within the epithelium in cardiac-type glands in biopsies from patients without Barrett's esophagus. Musashi-1 expression was present in Barrett's intestinal metaplasia and in dysplastic Barrett's in which the majority of epithelial cells in individual glands expressed this antigen. Expression of Musashi-1 was highest in esophageal adenocarcinoma, where it was most intense in glands that displayed features of early stages of adenocarcinoma formation. In contrast, Musashi-1 staining level was weaker in glands that displayed features of advanced adenocarcinoma. Double immunostaining with proliferating cell nuclear antigen showed low proliferation in the vast majority of Musashi-1+ cells. Musashi-1 mRNA expression levels were significantly higher in esophageal adenocarcinoma than in normal esophagus or Barrett's esophagus tissues. Dendritic cell-specific intercellular molecule-3 (ICAM-3)-grabbing nonintegrin (DC-SIGN) mRNA expression levels were significantly increased in both Barrett's tissues and adenocarcinoma tissues. Expression of the putative stem cell marker Musashi-1 is absent in normal squamous epithelium, weak in esophageal cardiac-type glands and Barrett's esophagus, and markedly increased in adenocarcinoma, especially in glands displaying features of early cancer development. Musashi-1 expressing cells may be significant in the etiology of Barrett's esophagus and adenocarcinoma, and perhaps even a cell of origin for this disease. We speculate that immune inflamm...

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Plant Heat-Shock Protein-Based Self-Adjuvanted Immunogens

Baschieri

2013

Molecular Vaccines

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Dendritic Cells and their Receptors in Antitumor Immune Response

Cited by 4 publications

References 173 publications

Natural killer (NK):dendritic cell (DC) cross talk induced by therapeutic monoclonal antibody triggers tumor antigen-specific T cell immunity

Natural killer (NK):dendritic cell (DC) cross talk induced by therapeutic monoclonal antibody triggers tumor antigen-specific T cell immunity

Expression of the putative stem cell marker Musashi-1 in Barrett's esophagus and esophageal adenocarcinoma

Plant Heat-Shock Protein-Based Self-Adjuvanted Immunogens

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