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Related Concept Videos

T Cell Activation and Clonal Selection01:22

T Cell Activation and Clonal Selection

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T cells are integral to our adaptive immune system, recognizing and effectively responding to foreign antigens. T cell activation and clonal selection are pivotal in orchestrating this immune response. This article elucidates these mechanisms, detailing the roles of cluster of differentiation (CD) markers, major histocompatibility complex (MHC) molecules, costimulatory signals, and the process of clonal selection.
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Immune Response Against Viral Pathogens01:29

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The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
NK Cells
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...
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B Cell Activation and Differentiation01:24

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The adaptive immune response, a sophisticated defense mechanism, relies on the activation and differentiation of B lymphocytes, or B cells. These processes enable our bodies to mount a tailored response against specific pathogens such as bacteria, free virus particles, toxins, and parasites.
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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Cytotoxic T Cells-mediated Immune Response01:27

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Cytotoxic T cells are a vital component of the immune system. They have the remarkable ability to identify and target antigens on infected or abnormal cells. These antigens often originate from intracellular pathogens such as viruses or abnormal proteins cancer cells produce.
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Cells of the Innate Immune Response01:28

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The innate immune response is an immediate and non-specific response against pathogens, acting swiftly to prevent the spread of infections. The primary cells involved in this response are phagocytes and natural killer (NK) cells.
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Peptide-based Identification of Functional Motifs and their Binding Partners
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NAD+ protects against EAE by regulating CD4+ T-cell differentiation.

Stefan G Tullius1, Hector Rodriguez Cetina Biefer2, Suyan Li3

  • 1Division of Transplant Surgery and Transplantation Surgery Research Laboratory, Department of Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.

Nature Communications
|October 8, 2014
PubMed
Summary
This summary is machine-generated.

Nicotinamide adenine dinucleotide (NAD(+)) halts experimental autoimmune encephalomyelitis (EAE), a multiple sclerosis model, by promoting immune balance. NAD(+) also aids tissue repair through remyelination and neuroregeneration, suggesting therapeutic potential for autoimmune diseases.

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Area of Science:

  • Immunology
  • Neuroscience
  • Metabolism

Background:

  • CD4(+) T cells play a critical role in autoimmune diseases like multiple sclerosis (MS).
  • Understanding immune regulation in autoimmunity is crucial for developing effective therapies.

Purpose of the Study:

  • To investigate the therapeutic potential of nicotinamide adenine dinucleotide (NAD(+)) in experimental autoimmune encephalomyelitis (EAE), a mouse model of MS.
  • To elucidate the mechanism by which NAD(+) modulates CD4(+) T-cell differentiation and immune responses.

Main Methods:

  • Administration of NAD(+) in a mouse model of MS (EAE).
  • Analysis of CD4(+) T-cell subsets, including IFNγ and IL-10 production.
  • Assessment of remyelination and neuroregeneration.
  • Investigation of NAD(+) regulation of T-cell differentiation via tryptophan hydroxylase-1 (Tph1).

Main Results:

  • NAD(+) treatment effectively blocked EAE progression and reversed disease severity.
  • NAD(+) induced immune homeostasis by promoting CD4(+)IFNγ(+)IL-10(+) T cells.
  • NAD(+) regulates CD4(+) T-cell differentiation through Tph1, independent of known transcription factors.
  • NAD(+) treatment promoted remyelination and neuroregeneration, restoring tissue integrity.

Conclusions:

  • NAD(+) demonstrates significant therapeutic potential for treating autoimmune diseases like MS.
  • NAD(+) acts via a novel pathway involving Tph1 to regulate CD4(+) T-cell differentiation and immune homeostasis.
  • NAD(+) promotes tissue repair mechanisms, including remyelination and neuroregeneration.