NDLI: Langerhans cells regulate cutaneous injury by licensing CD8 effector cells recruited to the skin

Content Provider	PubMed Central
Author	Bennett, Clare L. Farnaz, Fallah-arani Conlan, Thomas Trouillet, Celine Goold, Hugh Chorro, Laurent Barry, Flutter Means, Terry K. Geissmann, Frédéric Chakraverty, Ronjon
Copyright Year	2011
Abstract	Langerhans cells (LCs) are a distinct population of dendritic cells that form a contiguous network in the epidermis of the skin. Although LCs possess many of the properties of highly proficient dendritic cells, recent studies have indicated that they are not necessary to initiate cutaneous immunity. In this study, we used a tractable model of cutaneous GVHD, induced by topical application of a Toll-like receptor agonist, to explore the role of LCs in the development of tissue injury. By adapting this model to permit inducible and selective depletion of host LCs, we found that GVHD was significantly reduced when LCs were absent. However, LCs were not required either for CD8 T-cell activation within the draining lymph node or subsequent homing of effector cells to the epidermis. Instead, we found that LCs were necessary for inducing transcription of IFN-γ and other key effector molecules by donor CD8 cells in the epidermis, indicating that they license CD8 cells to induce epithelial injury. These data demonstrate a novel regulatory role for epidermal LCs during the effector phase of an inflammatory immune response in the skin.
Related Links	http://dx.doi.org/10.1182/blood-2011-01-329185
Starting Page	7063
File Format	PDF
ISSN	15280020
e-ISSN	15280020
Journal	Blood
Issue Number	26
Volume Number	117
Language	English
Publisher	American Society of Hematology
Publisher Date	2011-06-30
Access Restriction	Open
Rights Holder	American Society of Hematology
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cell Biology Hematology Biochemistry 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

IL-12 selectively programs effector pathways that are stably expressed in human CD8+ effector memory T cells in vivo

Engraftment of human central memory-derived effector CD8+ T cells in immunodeficient mice

Cross-priming CD8+ T cells by targeting antigens to human dendritic cells through DCIR

IL-15 administered by continuous infusion to rhesus macaques induces massive expansion of CD8+ T effector memory population in peripheral blood

Human effector CD8+ T cells derived from naive rather than memory subsets possess superior traits for adoptive immunotherapy

Interferon gamma licensing of human dendritic cells in T-helper–independent CD8+ alloimmunity

Skin-derived interleukin-7 contributes to the proliferation of lymphocytes in cutaneous T-cell lymphoma

Reciprocal responsiveness to interleukin-12 and interferon-α specifies human CD8+ effector versus central memory T-cell fates

Transition of late-stage effector T cells to CD27+ CD28+ tumor-reactive effector memory T cells in humans after adoptive cell transfer therapy

Langerhans cells regulate cutaneous injury by licensing CD8 effector cells recruited to the skin

Similar Documents

IL-12 selectively programs effector pathways that are stably expressed in human CD8+ effector memory T cells in vivo

Engraftment of human central memory-derived effector CD8+ T cells in immunodeficient mice

Cross-priming CD8+ T cells by targeting antigens to human dendritic cells through DCIR

IL-15 administered by continuous infusion to rhesus macaques induces massive expansion of CD8+ T effector memory population in peripheral blood

Human effector CD8+ T cells derived from naive rather than memory subsets possess superior traits for adoptive immunotherapy

Interferon gamma licensing of human dendritic cells in T-helper–independent CD8+ alloimmunity

Skin-derived interleukin-7 contributes to the proliferation of lymphocytes in cutaneous T-cell lymphoma

Reciprocal responsiveness to interleukin-12 and interferon-α specifies human CD8+ effector versus central memory T-cell fates

Transition of late-stage effector T cells to CD27+ CD28+ tumor-reactive effector memory T cells in humans after adoptive cell transfer therapy

Langerhans cells regulate cutaneous injury by licensing CD8 effector cells recruited to the skin