My hypothesis: The Hyper-IgE syndrome, also known as Job’s syndrome, is an immunodeficiency disease resulting from the lack of function of a single gene (gene ‘X’). This Hyper IgE/Job's syndrome or STAT3 deficiency(HIES) is caused by STAT3 gene mutation. STAT3 is a gene involved in major signal transduction pathways including wound healing, angiogenesis, immune response, and allergies. This genetic mutation is autosomal dominant in nature. The above mentioned are the most likely immune function impaired in the Gene X-deficient patients including immunity with eczematous and non-immunologic system disorders. Question: In a lab, histological examination of tongue sections from Candida albicans infected mice were examined, and the numbers of infiltrating leukocytes (white blood cells) were quantified in each microscopic field of each section, and the results are shown in the figure below. Do these data support or refute my hypothesis stated above?  Why or why not?

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Mitochondrial Mutations

A mitochondrion is a cellular organelle that serves as the site for cellular respiration and energy production (ATP or Adenosine Triphosphate). It is a double-membrane-bound organelle and is only present in eukaryotic cells.