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Longitudinal Analysis of Disease-Site Activities Impairing Wound Healing in Epidermolysis Bullosa and Development of Therapeutic Strategies

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Technical Report,01 Sep 2018,31 Aug 2019

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Thomas Jefferson University Philadelphia United States

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Development of chronic wounds is very common for patients affected by hereditary Epidermolysis Bullosa EB. To date, there is still a substantial gap in understanding of the cellular events occurring during progression of wounds from early to poorly healing, and chronic wounds. To understand the dynamics of the inflammatory infiltrates at EB skin wounds and, possibly, delineate leukocytic cells, which are responsible for stalled wound repair, we conducted comprehensive FACS-based assessment of leukocytic populations associated with different stages of EB wound progression. Our analysis has determined that EB skin wound bed is associated with CD11c antigen presenting cells 20 percent, CD11b mature neutrophils 38 percent and macrophages 7 percent, and T cells 40 percent. Remarkably, the majority of CD11c antigen presenting cells 80 percent, including CD207 Langerhans cells, express CD80 activation marker and the majority of the CD4 and CD8 T cells are represented by CD45RO effector T cells. In addition, our data demonstrated activation of adaptive immunity toward bacterial antigens in EB-associated wounds, immune-mediated targeting of infected host cells, and Treg-mediated inhibition of T cell responses toward bacterial antigens. Our findings suggest that adaptive immunity plays an important role in clearing bacterial infection in EB wounds.

Subject Categories:

  • Medicine and Medical Research
  • Weapons Effects (Biological)

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