NDLI: Characterizing tumor-promoting T cells in chemically induced cutaneous carcinogenesis

Content Provider	PubMed Central
Author	Roberts, Scott J. Ng, Bernice Y. Filler, Renata B. Lewis, Julia Glusac, Earl J. Hayday, Adrian C. Tigelaar, Robert E. Girardi, Michael
Copyright Year	2007
Abstract	There is a longstanding but poorly understood epidemiologic link between inflammation and cancer. Consistent with this, we previously showed that αβ T cell deficiency can increase resistance to chemical carcinogenesis initiated by 7,12-dimethylbenz[a]anthracene and promoted by phorbol 12-myristate 13-acetate. This provoked the hypothesis that αβ T cell deficiency removed T regulatory cells that limit the anti-tumor response or removed a specific tumor-promoting (T-pro) T cell population. Here we provide evidence for the latter, identifying a novel CD8+ subset that is a candidate for T-pro cells. We demonstrate that CD8 cell-deficient mice show substantially less tumor incidence and progression to carcinoma, whereas susceptibility is restored by CD8+ cell reconstitution. To characterize the putative T-pro cells, tumor-infiltrating lymphocytes were isolated from normal and CD4−/− mice, revealing an activated population of T cell receptor αβ+CD8+CD44+CD62L− cells expressing the inflammatory mediators IFNγ, TNFα, and cyclooxygenase-2, but deficient in perforin, relative to recirculating cells of equivalent phenotype. This novel population of CD8+ T cells has intriguing similarities with other lymphocytes that have been associated with tissue growth and invasiveness and has implications for inflammation-associated carcinogenesis, models of cancer immunosurveillance, and immunotherapeutic strategies.
Related Links	http://dx.doi.org/10.1073/pnas.0604982104
Ending Page	6775
Page Count	6
Starting Page	6770
File Format	PDF
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	16
Volume Number	104
Language	English
Publisher	National Academy of Sciences
Publisher Date	2007-04-17
Access Restriction	Open
Rights Holder	National Academy of Sciences
Subject Keyword	General Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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

Molecular Analysis of Tumor-Promoting CD8+ T Cells in Two-Stage Cutaneous Chemical Carcinogenesis

Accelerated chemically induced tumor development mediated by CD4+CD25+ regulatory T cells in wild-type hosts

Tumor-promoting role of TGFβ1 signaling in ultraviolet B-induced skin carcinogenesis is associated with cutaneous inflammation and lymph node migration of dermal dendritic cells

Tumor-promoting role of TGFβ1 signaling in ultraviolet B-induced skin carcinogenesis is associated with cutaneous inflammation and lymph node migration of dermal dendritic cells

B regulatory cells and the tumor-promoting actions of TNF-α during squamous carcinogenesis

B regulatory cells and the tumor-promoting actions of TNF- during squamous carcinogenesis.

Cyclin-dependent kinase 8 mediates chemotherapy-induced tumor-promoting paracrine activities

Antagonistic roles of CD4+ and CD8+ T-Cells in DMBA cutaneous carcinogenesis

Tumor sialylation impedes T cell mediated anti-tumor responses while promoting tumor associated-regulatory T cells

Characterizing tumor-promoting T cells in chemically induced cutaneous carcinogenesis

Similar Documents

Molecular Analysis of Tumor-Promoting CD8+ T Cells in Two-Stage Cutaneous Chemical Carcinogenesis

Accelerated chemically induced tumor development mediated by CD4+CD25+ regulatory T cells in wild-type hosts

Tumor-promoting role of TGFβ1 signaling in ultraviolet B-induced skin carcinogenesis is associated with cutaneous inflammation and lymph node migration of dermal dendritic cells

Tumor-promoting role of TGFβ1 signaling in ultraviolet B-induced skin carcinogenesis is associated with cutaneous inflammation and lymph node migration of dermal dendritic cells

B regulatory cells and the tumor-promoting actions of TNF-α during squamous carcinogenesis

B regulatory cells and the tumor-promoting actions of TNF- during squamous carcinogenesis.

Cyclin-dependent kinase 8 mediates chemotherapy-induced tumor-promoting paracrine activities

Antagonistic roles of CD4+ and CD8+ T-Cells in DMBA cutaneous carcinogenesis

Tumor sialylation impedes T cell mediated anti-tumor responses while promoting tumor associated-regulatory T cells

Characterizing tumor-promoting T cells in chemically induced cutaneous carcinogenesis