Figure 4 Paired Immunofluorescence staining for IgA and total SC, or for unoccupied and bound SC, in tissue sections of human colonic mucosa, (a) left part (red filtration) and right part (double exposure), comparable fields in adjacent sections of gland incubated with 'red' anti-SC and with 'red' anti-lgA + 'green' anti-SC, respectively. Prominent SC-containing granules are present in the Golgi zones, whereas the rest of the cytoplasm and the basolateral aspects of columnar epithelial cells are positive for both SC and IgA (mixed color). Goblet cells are devoid of both markers, (b) (red filtration), (c) (left part, double exposure), and (d) (green filtration), same field in a section of gland incubated with 'red' anti-l determinant (specific for unoccupied SC) + 'green' anti-A determinant (accessible on free as well as bound SC). The two antigenic determinants show distinct differential distribution with a relative dominance of I in the Golgi zones, and of A in the remaining cytoplasm and weakly also basolaterally. Right part of (c) (double exposure) shows a comparable field after prolonged exposure time for red (anti-l) emission. Note that neither of the two anti-SC reagents produced fluorescence of elements in the lamina propria. Original magnification x180. (See also color Plate 5B.)

such as interferon 7 (IFNy), interleukin 4 (IL-4) and tumor necrosis factor a (TNFa). Experiments with the HT-29 adenocarcinoma cell line have suggested that IFN7, IL-4 and TNFa all induce transcriptional upregulation of plgR, and IL-4 may additionally stabilize the specific message. We and others have recently cloned and characterized the promoter region of the SC/pIgR gene. DNA elements that bind transcription factors belonging to the basic helix-loop-helix leucine-zipper family or the interferon regulatory factor family appear important for constitutive or IFN7-enhanced transcription, respectively.

There thus appears to exist a positive immunoreg-ulatory link between the function of the plgR and a

Figure 5 (a) Paired immunofluorescence staining to demonstrate in vitro SC affinity to IgA immunocytes in section of human colonic mucosa preincubated with free SC followed by 'red' anti-SC + 'green' anti-lgA. Note in double exposure (center) that most IgA cells show varying degree of mixed color as evidence for binding of SC to cytoplasmic plgA, whereas a few cells (probably pure monomer producers) lack SC-binding capacity and are therefore only green. The purely red cells in the double exposure are SC-binding IgM immunocytes. The columnar epithelial cells of the glands at top and bottom contain innate SC and transport plgA; they therefore show mixed cytoplasmic color with the exception of the Golgi zones which contain SC but no IgA. Magnification x110. (b) Similar SC-affinity test on section of human salivary gland. Double exposure (center) shows various tints of yellow in IgA immunocytes located between acini (A) and duct (D); in several immunocytes the yellow color is restricted to areas close to the nucleus (arrow), suggesting accumulation of plgA. One immunocyte (at the bottom) is purely green, suggesting production of only monomeric IgA. Acini and duct are faintly double-stained for innate SC and translocated plgA. Magnification x430. (See also color Plate 5C.)

the magnitude of the local immune response. Our immunohistochemical observations on Sjogren's syndrome and chronic gastritis harmonize with this notion; signs of increased SC expression and enhanced uptake of IgA are seen in glandular structures surrounded by dense infiltrates of mononuclear cells. Similar epithelial features are seen in celiac disease; and enhanced external transport probably explains that there is little increase of the serum IgA level compared with the remarkably expanded jejunal IgA cell population. Nevertheless, the plgR-mediated epithelial transport capacity may be insufficient in certain patients with an unusual intestinal IgA cell expansion, resulting in excessive amounts of plgA in serum.

See also: Antibodies, secretion; IgA; IgM; Joining J chain; Mucosal immunity; Mucosa-associated lymphoid tissue (MALT).

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