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Related Concept Videos

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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Immunological memory, a pivotal pillar of the adaptive immune system, is responsible for the body's ability to remember and respond more swiftly and effectively to previously encountered pathogens. This remarkable feature is what makes vaccines so effective in preventing diseases.
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T Cell Types and Functions01:24

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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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The T and B lymphocytes of the adaptive immune system develop from common lymphoid progenitor cells in the bone marrow. These progenitors give rise to precursors that eventually develop into both T and B lymphocytes. As these precursors mature, they gain the ability to detect and respond to foreign antigens in the body, a process known as immunocompetence. Additionally, these precursors acquire self-tolerance, a process that ensures they do not react to self-antigens. This intricate system...
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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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The initiation of cell-mediated immunity can be observed as early as the third month of fetal growth, with active antibody-mediated immunity following approximately one month later.
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EBI2 Expression and Function: Robust in Memory Lymphocytes and Increased by Natalizumab in Multiple Sclerosis.

Aurélie S Clottu1, Amandine Mathias2, Andreas W Sailer3

  • 1Laboratories of Neuroimmunology, Neuroscience Research Center, Department of Clinical Neurosciences, Lausanne University Hospital, Chemin des Boveresses 155, 1066 Epalinges, Switzerland; Department of Pathology and Immunology, Geneva University Medical Center, Rue Michel-Servet 1, 1211 Geneva 4, Switzerland; Division of Immunology and Allergology, Department of Medical Specialties, Geneva University Hospitals, Rue Gabrielle-Perret-Gentil 4, 1211 Geneva 14, Switzerland.

Cell Reports
|January 5, 2017
PubMed
Summary

Epstein-Barr virus-induced gene 2 (EBI2) is functionally expressed on memory CD4+ T cells in multiple sclerosis (MS) patients. EBI2 enhances immune cell migration, offering a potential therapeutic target for MS and other autoimmune diseases.

Keywords:
G protein-coupled receptor Epstein-Barr virus-induced gene 2 (EBI2)lymphocyte traffickingmultiple sclerosisnatalizumaboxysterols

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Area of Science:

  • Immunology
  • Neuroscience
  • Cell Biology

Background:

  • Oxysterols and G protein-coupled receptor Epstein-Barr virus-induced gene 2 (EBI2) regulate immune cell migration.
  • This interaction is a target for multiple sclerosis (MS) treatments like natalizumab.
  • Previous studies showed EBI2-mediated migration of CD4+ T cells in a murine MS model.

Purpose of the Study:

  • To characterize the EBI2 expression profile in human lymphocytes from healthy and MS donors.
  • To investigate the functional role of EBI2 in human CD4+ T cell migration.
  • To assess EBI2 expression changes in response to natalizumab treatment.

Main Methods:

  • Flow cytometry to analyze EBI2 expression on human lymphocytes.
  • Functional assays to assess T cell migration.
  • Analysis of EBI2 expression in patients treated with natalizumab.

Main Results:

  • EBI2 is functionally expressed on human memory CD4+ T cells.
  • EBI2 expression is enhanced in CD4+ T cells from patients undergoing natalizumab treatment.
  • These findings highlight EBI2's role in human T cell migration, particularly in MS.

Conclusions:

  • EBI2 plays a significant role in human CD4+ T cell migration.
  • The EBI2 pathway is relevant in the context of multiple sclerosis.
  • Understanding EBI2 in autoimmunity could improve insights into MS pathophysiology.