API

Relationship: 835

Title

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Activation/Proliferation, T-cells leads to sensitisation, skin

Upstream event

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Activation/Proliferation, T-cells

Downstream event

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sensitisation, skin

Key Event Relationship Overview

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AOPs Referencing Relationship

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AOP Name Directness Weight of Evidence Quantitative Understanding
Covalent Protein binding leading to Skin Sensitisation directly leads to Strong

Taxonomic Applicability

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Sex Applicability

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Life Stage Applicability

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How Does This Key Event Relationship Work

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After recognition of a non-self peptide (i.e. foreign) presented by dendritic cells, T-cells are activated and form memory T-cell, which proliferate. If reactivated upon hapten presentation by skin dendritic cells, these memory T-cells will induce allergic contact dermatitis[1]).

This KER description is based only on the OECD document 2012 and needs updating.

Weight of Evidence

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Biological Plausibility

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It is well known, recognised and experimentally proved that skin sensitisation is a T-cell mediated immune response[1].

Empirical Support for Linkage

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Using dinitrofluorobenzene and mice models, it was shown that cutaneous contact with reactive antigen induces KC/CXC chemokine ligand 1 production and neutrophil infiltration in an antigen, dose-dependent manner. The intensity of neutrophil infiltration into cutaneous antigen challenge sites, in turn, controls the number of antigen-primed T cells recruited into the site and the magnitude of immune response elicited[2].

Uncertainties or Inconsistencies

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Quantitative Understanding of the Linkage

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Evidence Supporting Taxonomic Applicability

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References

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  1. 1.0 1.1 Vocanson M, Hennino A, Rozieres A, Poyet G, Nicolas JF. 2009. Effector and regulatory mechanisms in allergic contact dermatitis. Allergy 64: 1699-1714.
  2. Engeman T, Gorbachev AV, Kish DD, Fairchild RL. 2004. The intensity of neutrophil infiltration controls the number of antigen-primed CD8 T cells recruited into cutaneous antigen challenge sites. J. Leukocyte Biol. 76:941-949.