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Cells of the Adaptive Immune Response01:23

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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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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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Related Experiment Video

Updated: Jun 17, 2025

Isolation of Group 2 Innate Lymphoid Cells from Mouse Nasal Mucosa to Detect the Expression of CD226
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ILC2-derived LIF licences progress from tissue to systemic immunity.

Mayuri Gogoi1, Paula A Clark2, Ana C F Ferreira2

  • 1MRC Laboratory of Molecular Biology, Cambridge, UK. mgogoi@mrc-lmb.cam.ac.uk.

Nature
|August 7, 2024
PubMed
Summary
This summary is machine-generated.

Leukaemia inhibitory factor (LIF) from innate lymphoid cells (ILC2s) is essential for immune cells to leave the lungs and travel to lymph nodes. Without LIF, immune cell migration is blocked, impacting lung immunity and systemic responses.

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Area of Science:

  • Immunology
  • Cell Biology
  • Respiratory Medicine

Background:

  • Immune cell trafficking is crucial for surveillance and immune responses.
  • Adhesion and chemokine receptors guide immune cells to specific tissues and lymphatic system.
  • Group 2 innate lymphoid cells (ILC2s) play roles in tissue immunity.

Purpose of the Study:

  • To investigate the role of leukaemia inhibitory factor (LIF) produced by ILC2s in immune cell migration from the lungs.
  • To understand how LIF influences immune responses during viral infection and allergic challenge.
  • To elucidate the mechanism by which ILC2s regulate immune cell homing to lymph nodes.

Main Methods:

  • Investigated the impact of disrupted LIF production from ILC2s on immune cell migration.
  • Analyzed immune cell distribution in lungs and lymph nodes following viral infection and allergen challenge.
  • Examined the expression of chemokines (CCL21) and receptors (CCR7) in lymphatic endothelial cells and immune cells.

Main Results:

  • Disruption of LIF production by ILC2s prevents immune cells from migrating from the lungs to lymph nodes.
  • In the absence of LIF, plasmacytoid dendritic cells (pDCs) are retained in the lungs, enhancing local antiviral immunity.
  • Chronic allergen challenge with absent LIF leads to immune cell accumulation and tertiary lymphoid structure formation in the lungs.
  • ILC2-derived LIF induces CCL21 production in lymphatic endothelial cells, facilitating CCR7+ immune cell homing to lymph nodes.
  • Failure of immune cell migration to lymphatics results in compromised lymph node reactions.

Conclusions:

  • ILC2-derived LIF is a key regulator of immune cell egress from the lungs.
  • LIF controls the balance between tissue-localized immunity and systemic immune responses.
  • LIF production by ILC2s influences the immune system's response to both viral infections and allergens in the lungs.