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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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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.
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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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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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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 surveillance is an integral part of the innate immune system, involving the continuous monitoring of peripheral tissues to detect and respond to pathogens, infected cells, or cancerous cells. This surveillance is conducted primarily by natural killer (NK) cells and phagocytes, which employ distinct but complementary mechanisms to identify and eliminate threats.
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Group 2 Innate Lymphoid Cells Express Functional NKp30 Receptor Inducing Type 2 Cytokine Production.

Maryam Salimi1, Luzheng Xue2, Helen Jolin3

  • 1Medical Research Council Human Immunology Unit, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DS, United Kingdom;

Journal of Immunology (Baltimore, Md. : 1950)
|November 20, 2015
PubMed
Summary

Group 2 innate lymphoid cells (ILC2) express NKp30, a receptor that interacts with B7-H6 to trigger type 2 cytokine release. This pathway is implicated in atopic dermatitis and offers a therapeutic target.

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Area of Science:

  • Immunology
  • Cell Biology
  • Dermatology

Background:

  • Group 2 innate lymphoid cells (ILC2) are crucial for allergic inflammation, parasite defense, and tissue repair.
  • While soluble factors influence ILC2, their direct cellular interactions are less understood.
  • Natural cytotoxicity receptors (NCRs) are known in other ILC groups but not ILC2.

Purpose of the Study:

  • To investigate the expression and function of the NCR NKp30 on human ILC2.
  • To explore the role of the NKp30-B7-H6 interaction in ILC2 activation and cytokine production.
  • To assess the relevance of this pathway in atopic dermatitis.

Main Methods:

  • Flow cytometry and immunohistochemistry to detect NKp30 expression on ILC2.
  • In vitro co-culture assays to study NKp30-B7-H6 interactions and cytokine production.
  • Analysis of B7-H6 expression in lesional skin biopsies from atopic dermatitis patients.

Main Results:

  • A subset of human ILC2 expresses NKp30.
  • NKp30 engagement with its ligand B7-H6 induces rapid type 2 cytokine production by ILC2.
  • NKp30-mediated activation can be modulated by blocking antibodies and galectin-3.
  • B7-H6 expression is elevated in atopic dermatitis skin lesions and upregulated by inflammatory cytokines.

Conclusions:

  • NKp30-B7-H6 represents a novel cell-contact-dependent mechanism for ILC2 activation.
  • This interaction is a potential therapeutic target for atopic dermatitis and other allergic diseases.