NDLI: B Cells and Programmed Death-Ligand 2 Signaling Are Required for Maximal Interferon-γ Recall Response by Splenic CD4+ Memory T Cells of Mice Vaccinated with Mycobacterium tuberculosis Ag85B

Content Provider	PubMed Central
Author	Riccomi, Antonella Palma, Carla
Editor	Giovanni, Delogu
Copyright Year	2015
Abstract	CD4+ T cells producing interferon-γ are crucial for protection against Mycobacterium tuberculosis infection and are the cornerstone of tuberculosis vaccination and immunological diagnostic assays. Since emerging evidence indicates that B cells can modulate T cell responses to M. tuberculosis infection, we investigated the contribution of B cells in regulating interferon-γ recall response by memory Thelper1 cells specific for Ag85B, a leading candidate for tuberculosis sub-unit vaccines. We found that B cells were able to maximize the reactivation of CD4+ memory T cells and the interferon-γ response against ex vivo antigen recall in spleens of mice vaccinated with Ag85B. B cell-mediated increase of interferon-γ response was particular evident for high interferon-γ producer CD4+ memory T cells, likely because those T cells were required for triggering and amplification of B cell activation. A positive-feedback loop of mutual activation between B cells, not necessarily antigen-experienced but with integral phosphatidylinositol-3 kinase (PI3K) pathway and a peculiar interferon-γ-producing CD4highT cell subset was established. Programed death-ligand 2 (PD-L2), expressed both on B and the highly activated CD4high T cells, contributed to the increase of interferon-γ recall response through a PD1-independent pathway. In B cell-deficient mice, interferon-γ production and activation of Ag85B-specific CD4+ T cells were blunted against ex vivo antigen recall but these responses could be restored by adding B cells. On the other hand, B cells appeared to down-regulate interleukin-22 recall response. Our data point out that nature of antigen presenting cells determines quality and size of T cell cytokine recall responses. Thus, antigen presenting cells, including B cells, deserve to be considered for a better prediction of cytokine responses by peripheral memory T cells specific for M. tuberculosis antigens. We also invite to consider B cells, PD-L2 and PI3K as potential targets for therapeutic modulation of T cell cytokine responses for tuberculosis control.
Related Links	http://dx.doi.org/10.1371/journal.pone.0137783
Starting Page	137783
File Format	PDF
ISSN	19326203
e-ISSN	19326203
Journal	PLoS ONE
Issue Number	9
Volume Number	10
Language	English
Publisher	Public Library of Science
Publisher Date	2015-09-01
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

Inhibition of Programmed Death 1 Ligand 1 on Dendritic Cells Enhances Mycobacterium-Mediated Interferon γ (IFN-γ) Production Without Modulating the Frequencies of IFN-γ–Producing CD4+ T Cells

Inhibiting the Programmed Death 1 Pathway Rescues Mycobacterium tuberculosis–Specific Interferon γ–Producing T Cells From Apoptosis in Patients With Pulmonary Tuberculosis

OX40 ligand and programmed cell death 1 ligand 2 expression on inflammatory dendritic cells regulates CD4 T cell cytokine production in the lung during viral disease.

Mycobacterium tuberculosis–Induced Reduction of Interferon γ–Producing CD4 T Cells in Active Tuberculosis

Programmed death 1 ligand signaling regulates the generation of adaptive Foxp3+CD4+ regulatory T cells

Major histocompatibility complex class I-restricted T cells are required for resistance to Mycobacterium tuberculosis infection.

Interferon-γ Receptor Signaling in Dendritic Cells Restrains Spontaneous Proliferation of CD4+ T Cells in Chronic Lymphopenic Mice

Cutting edge: Direct recognition of infected cells by CD4 T cells is required for control of intracellular Mycobacterium tuberculosis in vivo.

T cell-dependent IgM memory B cells generated during bacterial infection are required for IgG responses to antigen challenge.

B Cells and Programmed Death-Ligand 2 Signaling Are Required for Maximal Interferon-γ Recall Response by Splenic CD4+ Memory T Cells of Mice Vaccinated with Mycobacterium tuberculosis Ag85B

Similar Documents

Inhibition of Programmed Death 1 Ligand 1 on Dendritic Cells Enhances Mycobacterium-Mediated Interferon γ (IFN-γ) Production Without Modulating the Frequencies of IFN-γ–Producing CD4+ T Cells

Inhibiting the Programmed Death 1 Pathway Rescues Mycobacterium tuberculosis–Specific Interferon γ–Producing T Cells From Apoptosis in Patients With Pulmonary Tuberculosis

OX40 ligand and programmed cell death 1 ligand 2 expression on inflammatory dendritic cells regulates CD4 T cell cytokine production in the lung during viral disease.

Mycobacterium tuberculosis–Induced Reduction of Interferon γ–Producing CD4 T Cells in Active Tuberculosis

Programmed death 1 ligand signaling regulates the generation of adaptive Foxp3+CD4+ regulatory T cells

Major histocompatibility complex class I-restricted T cells are required for resistance to Mycobacterium tuberculosis infection.

Interferon-γ Receptor Signaling in Dendritic Cells Restrains Spontaneous Proliferation of CD4+ T Cells in Chronic Lymphopenic Mice

Cutting edge: Direct recognition of infected cells by CD4 T cells is required for control of intracellular Mycobacterium tuberculosis in vivo.

T cell-dependent IgM memory B cells generated during bacterial infection are required for IgG responses to antigen challenge.

B Cells and Programmed Death-Ligand 2 Signaling Are Required for Maximal Interferon-γ Recall Response by Splenic CD4+ Memory T Cells of Mice Vaccinated with Mycobacterium tuberculosis Ag85B