NDLI: T Helper Subsets, Peripheral Plasticity, and the Acute Phase Protein, α1-Antitrypsin

Content Provider	PubMed Central
Author	Baranovski, Boris M. Freixo-lima, Gabriella S. Lewis, Eli C. Rider, Peleg
Copyright Year	2015
Abstract	The traditional model of T helper differentiation describes the naïve T cell as choosing one of several subsets upon stimulation and an added reciprocal inhibition aimed at maintaining the chosen subset. However, to date, evidence is mounting to support the presence of subset plasticity. This is, presumably, aimed at fine-tuning adaptive immune responses according to local signals. Reprograming of cell phenotype is made possible by changes in activation of master transcription factors, employing epigenetic modifications that preserve a flexible mode, permitting a shift between activation and silencing of genes. The acute phase response represents an example of peripheral changes that are critical in modulating T cell responses. α1-antitrypsin (AAT) belongs to the acute phase responses and has recently surfaced as a tolerogenic agent in the context of adaptive immune responses. Nonetheless, AAT does not inhibit T cell responses, nor does it shutdown inflammation per se; rather, it appears that AAT targets non-T cell immunocytes towards changing the cytokine environment of T cells, thus promoting a regulatory T cell profile. The present review focuses on this intriguing two-way communication between innate and adaptive entities, a crosstalk that holds important implications on potential therapies for a multitude of immune disorders.
Related Links	http://dx.doi.org/10.1155/2015/184574
Starting Page	184574
File Format	PDF
ISSN	23146141
e-ISSN	23146141
Journal	BioMed Research International
Volume Number	2015
Language	English
Publisher	Hindawi Publishing Corporation
Publisher Date	2015-01-01
Access Restriction	Open
Rights Holder	Hindawi Publishing Corporation
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Immunology and Microbiology Medicine Biochemistry, Genetics and Molecular Biology

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

T Helper Lymphocyte Subsets and Plasticity in Autoimmunity and Cancer: An Overview

Acute-Phase Protein α1-Antitrypsin Inhibits Neutrophil Calpain I and Induces Random Migration

Functional and Phenotypic Plasticity of CD4+ T Cell Subsets

Tailored Immune Responses: Novel Effector Helper T Cell Subsets in Protective Immunity

Mysteries of α1-antitrypsin deficiency: emerging therapeutic strategies for a challenging disease

The structural diversity in α1-antitrypsin misfolding

Nine lives: plasticity among T helper cell subsets

Increased Peripheral Proinflammatory T Helper Subsets Contribute to Cardiovascular Complications in Diabetic Patients

Retarded protein folding of deficient human α1-antitrypsin D256V and L41P variants

T Helper Subsets, Peripheral Plasticity, and the Acute Phase Protein, α1-Antitrypsin

Similar Documents

T Helper Lymphocyte Subsets and Plasticity in Autoimmunity and Cancer: An Overview

Acute-Phase Protein α1-Antitrypsin Inhibits Neutrophil Calpain I and Induces Random Migration

Functional and Phenotypic Plasticity of CD4+ T Cell Subsets

Tailored Immune Responses: Novel Effector Helper T Cell Subsets in Protective Immunity

Mysteries of α1-antitrypsin deficiency: emerging therapeutic strategies for a challenging disease

The structural diversity in α1-antitrypsin misfolding

Nine lives: plasticity among T helper cell subsets

Increased Peripheral Proinflammatory T Helper Subsets Contribute to Cardiovascular Complications in Diabetic Patients

Retarded protein folding of deficient human α1-antitrypsin D256V and L41P variants

T Helper Subsets, Peripheral Plasticity, and the Acute Phase Protein, α1-Antitrypsin