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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 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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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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Affinity-coupled CCL22 promotes positive selection in germinal centres.

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Germinal center B cells use chemokines CCL22 and CCL17 to attract follicular helper T (TFH) cells, ensuring high-affinity B cells receive preferential T cell help for effective antibody affinity maturation.

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Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Antibody affinity maturation occurs in germinal centers (GCs) through positive selection of B cells with higher affinity B cell receptors.
  • This selection relies on B cells presenting more antigen to follicular helper T (TFH) cells and receiving enhanced T cell help.
  • The dynamic GC environment poses challenges for sustained B cell-TFH cell interactions, making the mechanism of focused T cell help unclear.

Purpose of the Study:

  • To elucidate the mechanism by which T cell help is cumulatively focused onto rare, high-affinity B cell clones within germinal centers.
  • To investigate the role of chemokines in mediating intercellular communication and T cell help during the GC response.
  • To understand how B cell affinity influences the attraction of TFH cells and subsequent selection.

Main Methods:

  • Investigated chemokine (CCL22, CCL17) and receptor (CCR4) expression in GC B cells and TFH cells.
  • Utilized genetic ablation of CCL22 and CCL17 in B cells to assess their impact on GC formation and affinity maturation.
  • Assessed the effect of TFH cell modulation on CCL22 expression in GC B cells.
  • Compared the competitive fitness of wild-type B cells versus B cells lacking CCL22 and CCL17 in a GC response.

Main Results:

  • GC B cells upregulate CCL22 and CCL17 upon CD40 stimulation, attracting TFH cells via CCR4.
  • Higher antigen-binding affinity in GC B cells correlates with increased CCL22 expression, highlighting these cells for T cell help.
  • TFH cell activity directly influences CCL22 expression by GC B cells, establishing a feedback circuit.
  • Ablation of CCL22 and CCL17 impairs B cell affinity maturation and reduces T cell help, hindering GC participation and plasma cell development.

Conclusions:

  • A chemokine-mediated circuit, involving CCL22/CCL17 and CCR4, spatiotemporally orchestrates GC positive selection by preferentially directing T cell help to high-affinity B cells.
  • This mechanism ensures efficient antibody affinity maturation by linking recent T cell help to the ability to attract further help.
  • The study reveals a novel principle for focusing immune cell interactions within the complex GC microenvironment.