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Invariant natural killer T cells recognize glycolipids from pathogenic Gram-positive bacteria

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TLDR
The results show how microbial lipids position the sugar for recognition by the invariant TCR and extend the range of microbes recognized by this conserved TCR to several clinically important bacteria.
Abstract
Natural killer T cells (NKT cells) recognize glycolipid antigens presented by CD1d. These cells express an evolutionarily conserved, invariant T cell antigen receptor (TCR), but the forces that drive TCR conservation have remained uncertain. Here we show that NKT cells recognized diacylglycerol-containing glycolipids from Streptococcus pneumoniae, the leading cause of community-acquired pneumonia, and group B Streptococcus, which causes neonatal sepsis and meningitis. Furthermore, CD1d-dependent responses by NKT cells were required for activation and host protection. The glycolipid response was dependent on vaccenic acid, which is present in low concentrations in mammalian cells. Our results show how microbial lipids position the sugar for recognition by the invariant TCR and, most notably, extend the range of microbes recognized by this conserved TCR to several clinically important bacteria.

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Journal ArticleDOI

Evolution of nonclassical MHC-dependent invariant T cells

TL;DR: The current understanding of a nonclassical MHC class I-restricted iT cell population in the amphibian Xenopus laevis is reviewed, with parallels with the mammalian iNKT and MAIT cells underline the crucial biological roles of these evolutionarily ancient immune subsets.
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Aberrant presentation of self-lipids by autoimmune B cells depletes peripheral iNKT cells

TL;DR: Findings unveil a critical link between autoimmunity, B cell lipidome, and the maintenance of peripheral iNKT cells and highlight an essential homeostatic function of B cells beyond antibody production.
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Group B Streptococcus Induces a Robust IFN-γ Response by CD4(+) T Cells in an In Vitro and In Vivo Model.

TL;DR: In this article, the authors evaluated CD4+ T cell activation profiles in response to Group B Streptococcus (GBS) serotype III infection through in vivo, ex vivo, and in vitro approaches.
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From Lysosomal Storage Diseases to NKT Cell Activation and Back

TL;DR: The current knowledge about NKT cells in the context of LSDs is reviewed, including the alterations detected, the proposed mechanisms to explain these defects, and the relevance of these findings for disease pathology.
References
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Journal Article

Prevention of perinatal group B streptococcal disease. Revised guidelines from CDC.

TL;DR: Although universal screening for GBS colonization is anticipated to result in further reductions in the burden of GBS disease, the need to monitor for potential adverse consequences of intrapartum antibiotic use, such as emergence of bacterial antimicrobial resistance or increased incidence or severity of non-GBS neonatal pathogens, continues.
Journal ArticleDOI

Innate Immunity: The Virtues of a Nonclonal System of Recognition

TL;DR: Characterization of the nonclonal receptors of the innate immune system responsible for the adjuvant activity, and, evidently, for the associated side effects, would provide a powerful alternative approach, which would ultimately allow one to target these receptors directly.
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CD1d-restricted and TCR-mediated activation of valpha14 NKT cells by glycosylceramides.

TL;DR: Glycosylceramide-mediated proliferative responses of Valpha14 NKT cells were abrogated by treatment with chloroquine-concanamycin A or by monoclonal antibodies against CD1d/Vbeta8, CD40/CD40L, or B7/CTLA-4/CD28, but not by interference with the function of a transporter-associated protein.
Journal ArticleDOI

The global burden of group A streptococcal diseases

TL;DR: The need to reinforce current control strategies, develop new primary prevention strategies, and collect better data from developing countries for most diseases is highlighted, as GAS is an important cause of morbidity and mortality.
Journal ArticleDOI

Burden of disease caused by Streptococcus pneumoniae in children younger than 5 years: global estimates

TL;DR: The burden of pneumococcal pneumonia is measured by applying the proportion of pneumonia cases caused by S pneumoniae derived from efficacy estimates from vaccine trials to WHO country-specific estimates of all-cause pneumonia cases and deaths, using disease incidence and case-fatality data from a systematic literature review.
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