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An antigen is any substance the immune system identifies as foreign and potentially harmful to the body, prompting an immune response. Antigens have two functional properties: immunogenicity and reactivity. Immunogenicity is the ability of an antigen to stimulate a specific immune response. At the same time, reactivity describes the antigen's ability to react with the cells and antibodies produced in response to it.
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MHC molecules are key players in the immune response, enabling T cells to recognize and respond to specific antigens. They are present on the surface of all nucleated cells in the body and are instrumental in presenting antigens to T cells and activating them. T cells recognize the MHC-antigen complex and initiate an immune response. MHC class I and MHC class II are two main types of MHC molecules, each associated with a distinct antigen processing pathway.
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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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Human Keratinocyte Response to Superantigens.

Patrick M Schlievert1, Francoise A Gourronc2, Donald Y M Leung3

  • 1Department of Microbiology and Immunology, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA patrick-schlievert@uiowa.edu.

Msphere
|October 8, 2020
PubMed
Summary

Human skin pathogens Staphylococcus aureus and Streptococcus pyogenes release superantigens that trigger inflammation. Our study shows these toxins activate keratinocytes, leading to chemokine production and potentially harmful inflammatory responses on the skin.

Keywords:
RNA-seqStaphylococcus aureusStreptococcus pyogenescytokineskeratinocytesuperantigen

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Area of Science:

  • Microbiology and Immunology
  • Dermatology
  • Molecular Biology

Background:

  • Staphylococcus aureus and Streptococcus pyogenes are major human pathogens causing skin infections.
  • These bacteria secrete superantigens (e.g., TSST-1, SEs, SPEs) implicated in disease pathogenesis.
  • Human keratinocytes are the primary cells on the skin to encounter these superantigens.

Purpose of the Study:

  • To investigate the transcriptomic response of human primary keratinocytes to TSST-1 and SEB.
  • To identify specific genes and pathways affected by superantigen exposure.
  • To assess the production of chemokines by keratinocytes upon exposure to various superantigens.

Main Methods:

  • Transcriptome sequencing (RNA-seq) was used to analyze gene expression changes in human primary keratinocytes.
  • Cells were treated with TSST-1 and staphylococcal enterotoxin B (SEB).
  • Gene expression was analyzed for differential expression (≥2-fold change) and overlap between treatments.
  • Chemokine production (IL-8, MIP-3α, IL-33) was measured in response to superantigens in an immortalized keratinocyte line.

Main Results:

  • TSST-1 and SEB induced significant differential gene expression in keratinocytes, with thousands of genes upregulated and downregulated.
  • A substantial overlap in gene expression changes was observed between TSST-1 and SEB treatments.
  • Upregulated genes were enriched in pathways related to chemokine production and inflammation.
  • TSST-1, SEB, SPEA, and SPEC stimulated the production of key chemokines like IL-8.

Conclusions:

  • Human keratinocytes mount a significant transcriptional response to staphylococcal and streptococcal superantigens.
  • Superantigen exposure leads to the production of chemokines, initiating an inflammatory cascade.
  • This inflammation may compromise the skin barrier, potentially exacerbating infections.