NDLI: Blockade of IL-10 signaling during bacillus Calmette-Guérin vaccination enhances and sustains Th1, Th17, and innate lymphoid IFN-Î³ and IL-17 responses and increases protection to Mycobacterium tuberculosis infection.

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Blockade of IL-10 signaling during bacillus Calmette-Guérin vaccination enhances and sustains Th1, Th17, and innate lymphoid IFN-Î³ and IL-17 responses and increases protection to Mycobacterium tuberculosis infection.

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Blockade of IL-10 signaling during bacillus Calmette-Guérin vaccination enhances and sustains Th1, Th17, and innate lymphoid IFN-Î³ and IL-17 responses and increases protection to Mycobacterium tuberculosis infection.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Redford, Paul S. Stavropoulos, Evangelos O'Garra, Anne Bancroft, Gregory J. Pitt, Jonathan M. Beebe, Amy M. Young, Douglas B.
Description	Country affiliation: United kingdom Author Affiliation: Pitt JM ( Division of Immunoregulation, Medical Research Council National Institute for Medical Research, London NW7 1AA, United Kingdom.)
Abstract	Vaccination with Mycobacterium bovis bacillus Calmette-Guérin (BCG) remains the only prophylactic vaccine against tuberculosis, caused by Mycobacterium tuberculosis, but gives variable protection against pulmonary disease. The generation of host Th1 responses following BCG vaccination is accepted as the major mechanism of protection against M. tuberculosis infection. Early production of IL-17 in the lungs following M. tuberculosis challenge of mice previously vaccinated with M. tuberculosis peptides in adjuvant has been shown to be required for efficient Th1 cell recruitment. IL-10 regulates various processes involved in generation of Th1 and Th17 responses. Previous studies have shown IL-10 as a negative regulator of the immune response to primary M. tuberculosis infection, with Il10(-/-) mice having reduced lung bacterial loads. In this study we show that inhibition of IL-10 signaling during BCG vaccination enhances host-generated Ag-specific IFN-Î³ and IL-17A responses, and that this regimen gives significantly greater protection against aerogenic M. tuberculosis challenge in both susceptible and relatively resistant strains of mice. In M. tuberculosis-susceptible CBA/J mice, Ab blockade of IL-10R specifically during BCG vaccination resulted in additional protection against M. tuberculosis challenge of >1-log(10) compared with equivalent isotype-treated controls. The protection observed following BCG vaccination concurrent with anti-IL-10R mAb treatment was sustained through chronic M. tuberculosis infection and correlated with enhanced lung Th1 and Th17 responses and increased IFN-Î³ and IL-17A production by Î³Î´ T cells and an innate-like Thy1.2(+)CD3(-) lymphoid population. We show that IL-10 inhibits optimal BCG-elicited protection, therefore suggesting that antagonists of IL-10 may be of great benefit as adjuvants in preventive vaccination against tuberculosis.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1201061
Journal	The Journal of Immunology
Issue Number	8
Volume Number	189
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-10-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Bcg Vaccine Immunology Interferon-gamma Biosynthesis Interleukin-10 Antagonists & Inhibitors Interleukin-17 Signal Transduction Th1 Cells Th17 Cells Tuberculosis, Pulmonary Animals Antibodies, Blocking Administration & Dosage Benzamides Cells, Cultured Imatinib Mesylate Immunity, Innate Metabolism Physiology Mice Mice, Inbred C57bl Mice, Inbred Cba Mice, Knockout Piperazines Pyrimidines Receptors, Interleukin-10 T-lymphocyte Subsets Microbiology Prevention & Control Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Blockade of IL-10 signaling during BCG vaccination enhances and sustains Th1, Th17, and innate lymphoid IFN-γ and IL-17 responses and increases protection to Mycobacterium tuberculosis infection

Infection Mycobacterium tuberculosis Protection to and IL-17 Responses and Increases γ IFN-Sustains Th 1 , Th 17 , and Innate Lymphoid Calmette-Guérin Vaccination Enhances and Blockade of IL-10 Signaling during Bacillus

Differential Responsiveness of Innate-like IL-17- and IFN-Î³-Producing Î³Î´ T Cells to Homeostatic Cytokines.

IL-10 Receptor Blockade Delivered Simultaneously with Bacillus Calmette–Guérin Vaccination Sustains Long-Term Protection against Mycobacterium tuberculosis Infection in Mice

Blockade of IL-10 signaling during BCG vaccination enhances and sustains Th 1 , Th 17 , and innate lymphoid IFN-γ and IL-17 responses and increases protection to Mycobacterium tuberculosis infection

Epidermal CCR6+ Î³Î´ T cells are major producers of IL-22 and IL-17 in a murine model of psoriasiform dermatitis.

Th17 Cells Induce Colitis and Promote Th1 Cell Responses through IL-17 Induction of Innate IL-12 and IL-23 Production

The Antiasthma Effect of Neonatal BCG Vaccination Does Not Depend on the Th17/Th1 but IL-17/IFN-γ Balance in a BALB/c Mouse Asthma Model

IFN- induces IL-10 production and tilt the balance between Th1 and Th17 in Behçet disease.

Blockade of IL-10 signaling during bacillus Calmette-Guérin vaccination enhances and sustains Th1, Th17, and innate lymphoid IFN-Î³ and IL-17 responses and increases protection to Mycobacterium tuberculosis infection.

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