NDLI: Subcapsular Sinus Macrophage Fragmentation and CD169+ Bleb Acquisition by Closely Associated IL-17-Committed Innate-Like Lymphocytes

Content Provider	PubMed Central
Author	Gray, Elizabeth E. Friend, Sherree Suzuki, Kazuhiro Phan, Tri Giang Cyster, Jason G.
Editor	Niess, Jan-hendrik
Copyright Year	2012
Abstract	Subcapsular sinus macrophages (SSMs) in lymph nodes are rapidly exposed to antigens arriving in afferent lymph and have a role in their capture and display to B cells. In tissue sections SSMs exhibit long cellular processes and express high amounts of CD169. Here, we show that many of the cells present in lymph node cell suspensions that stain for CD169 are not macrophages but lymphocytes that have acquired SSM-derived membrane blebs. The CD169 bleb+ lymphocytes are enriched for IL-17 committed IL-7RαhiCCR6+ T cells and NK cells. In addition, the CD169 staining detected on small numbers of CD11chi dendritic cells is frequently associated with membrane blebs. Counter intuitively the CD169 bleb+ lymphocytes are mostly CD4 and CD8 negative whereas many SSMs express CD4. In situ, many IL-7Rαhi cells are present at the subcapsular sinus and interfollicular regions and migrate in close association with CD169+ macrophages. These findings suggest SSMs undergo fragmentation during tissue preparation and release blebs that are acquired by closely associated cells. They also suggest an intimate crosstalk between SSMs and IL-17 committed innate-like lymphocytes that may help provide early protection of the lymph node against lymph-borne invaders.
Related Links	http://dx.doi.org/10.1371/journal.pone.0038258
Starting Page	38258
File Format	PDF
ISSN	19326203
e-ISSN	19326203
Journal	PLoS ONE
Issue Number	6
Volume Number	7
Language	English
Publisher	Public Library of Science
Publisher Date	2012-06-01
Access Restriction	Open
Rights Holder	Public Library of Science
Subject Keyword	Biochemistry, Genetics and Molecular Biology(all) Agricultural and Biological Sciences(all) Medicine(all) 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

Tumor-Like Stem Cells Derived from Human Keloid Are Governed by the Inflammatory Niche Driven by IL-17/IL-6 Axis

Differential Induction of TLR3-Dependent Innate Immune Signaling by Closely Related Parasite Species

MyD88 Associated ROS Generation Is Crucial for Lactobacillus Induced IL-12 Production in Macrophage

Lymphatic Endothelial Cells Are Essential Components of the Subcapsular Sinus Macrophage Niche

Migratory and adhesive cues controlling innate-like lymphocyte surveillance of the pathogen-exposed surface of the lymph node

TLR7 Controls VSV Replication in CD169+ SCS Macrophages and Associated Viral Neuroinvasion

Lymph Node Subcapsular Sinus Macrophages as the Frontline of Lymphatic Immune Defense

IL-22 Is Produced by Innate Lymphoid Cells and Limits Inflammation in Allergic Airway Disease

Differential Expression of Iron Acquisition Genes by Brucella melitensis and Brucella canis during Macrophage Infection

Subcapsular Sinus Macrophage Fragmentation and CD169+ Bleb Acquisition by Closely Associated IL-17-Committed Innate-Like Lymphocytes

Similar Documents

Tumor-Like Stem Cells Derived from Human Keloid Are Governed by the Inflammatory Niche Driven by IL-17/IL-6 Axis

Differential Induction of TLR3-Dependent Innate Immune Signaling by Closely Related Parasite Species

MyD88 Associated ROS Generation Is Crucial for Lactobacillus Induced IL-12 Production in Macrophage

Lymphatic Endothelial Cells Are Essential Components of the Subcapsular Sinus Macrophage Niche

Migratory and adhesive cues controlling innate-like lymphocyte surveillance of the pathogen-exposed surface of the lymph node

TLR7 Controls VSV Replication in CD169+ SCS Macrophages and Associated Viral Neuroinvasion

Lymph Node Subcapsular Sinus Macrophages as the Frontline of Lymphatic Immune Defense

IL-22 Is Produced by Innate Lymphoid Cells and Limits Inflammation in Allergic Airway Disease

Differential Expression of Iron Acquisition Genes by Brucella melitensis and Brucella canis during Macrophage Infection

Subcapsular Sinus Macrophage Fragmentation and CD169+ Bleb Acquisition by Closely Associated IL-17-Committed Innate-Like Lymphocytes