Regulatory T‐cells in alopecia areata

  • Jodi J. Speiser
    Department of Pathology Loyola University Medical Center Maywood Illinois
  • Dana Mondo
    Department of Pathology Loyola University Medical Center Maywood Illinois
  • Vikas Mehta
    Department of Pathology Loyola University Medical Center Maywood Illinois
  • Sheela A. Marcial
    Department of Pathology Loyola University Medical Center Maywood Illinois
  • Ameet Kini
    Department of Pathology Loyola University Medical Center Maywood Illinois
  • Kelli A. Hutchens
    Department of Pathology Loyola University Medical Center Maywood Illinois

Description

<jats:title>Abstract</jats:title><jats:sec><jats:title>Background</jats:title><jats:p>Alopecia areata (AA) is believed to have an autoimmune mechanism in which the hair follicles are targeted by CD4+ and CD8+ lymphocytes. Studies investigating the autoimmune mechanism of other cutaneous diseases, including vitiligo, showed that <jats:italic>T</jats:italic><jats:sub>reg</jats:sub> is a component of cutaneous immune privilege. Our study uses immunohistochemical staining in formalin‐fixed, paraffin‐embedded tissue to examine the percentage of CD4<jats:sup>+</jats:sup>FoxP3<jats:sup>+</jats:sup>, CD25<jats:sup>+</jats:sup>FoxP3<jats:sup>+</jats:sup>, and CD8<jats:sup>+</jats:sup>FoxP3<jats:sup>+</jats:sup> <jats:italic>T</jats:italic><jats:sub>reg</jats:sub> in AA in human specimens.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Immunohistochemical double staining for CD4<jats:sup>+</jats:sup>FoxP3<jats:sup>+</jats:sup>, CD25<jats:sup>+</jats:sup>FoxP3<jats:sup>+</jats:sup>, and CD8<jats:sup>+</jats:sup>FoxP3<jats:sup>+</jats:sup> was performed on 12 AA cases and 12 other autoimmune and non‐autoimmune cutaneous diseases. The frequency of CD4<jats:sup>+</jats:sup>FoxP3<jats:sup>+</jats:sup>, CD25<jats:sup>+</jats:sup>FoxP3<jats:sup>+</jats:sup>, and CD8<jats:sup>+</jats:sup> FoxP3<jats:sup>+</jats:sup> <jats:italic>T</jats:italic><jats:sub>reg</jats:sub> was counted and expressed as a percentage of total CD4<jats:sup>+</jats:sup>, CD25<jats:sup>+</jats:sup>, and CD8<jats:sup>+</jats:sup> lymphocytes, respectively, in order to account for intersample inflammatory response variability.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>There was a significant reduction in the mean frequency of CD4<jats:sup>+</jats:sup> FoxP3<jats:sup>+</jats:sup> and CD25<jats:sup>+</jats:sup> FoxP3<jats:sup>+</jats:sup> in AA when compared to other autoimmune and non‐autoimmune cutaneous diseases.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p> <jats:italic>T</jats:italic><jats:sub>reg</jats:sub> is significantly lower in AA when compared to other cutaneous diseases. Additionally, this immunohistochemical‐staining protocol may be useful to evaluate <jats:italic>T</jats:italic><jats:sub>reg</jats:sub> in formalin‐fixed, paraffin‐embedded specimens for other cutaneous diseases. Studies examining <jats:italic>T</jats:italic><jats:sub>reg</jats:sub> in AA and other cutaneous diseases may have implications for future interventions.</jats:p></jats:sec>

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