Immunocytochemistry of Band 3 Protein in Kidney and Other Tissues of Control and Cystic Fibrosis Patients

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Abstract
Current evidence indicates that the underlying genetic defect in cystic fibrosis (CF) results in defective chloride transport, and more specifically, chloride impermeability. However, recent consideration has been given to a possible defect in band 3 protein at CF-affected sites. In an effort to determine a possible role for band 3, an anion exchange channel protein, a series of immunocytochemical localizations was performed. Immunocytochemical staining for the anion channel band 3, 43K, in normal and CF human kidney was confined to erythrocytes, glomerular podocytes, the basal region of half of the cells of the initial connecting segment of cortical collecting ducts, and a minority of cells in medullary ray-collecting ducts. Erythrocytes alone evidenced immunoreactivity for band 3 protein in human pancreas, submandibular gland, trachea, and lung. In all cases, specimens from patients with CF stained like those from control subjects for band 3. Abnormal CI- transport in CF tissues is not reflected in altered band 3, 43K, localizations.

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