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Molecular-Cellular Interactions in the Secretory IgA System

  • S. S. Crago
  • S. J. Prince
  • R. Kulhavy
  • J. Mestecky
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 107)

Abstract

The appearance of secretory-IgA (s-IgA) in external secretions is the result of the interaction between two cell types: plasma cells, which produce polymeric IgA (with J chain), and epithelial cells, which produce secretory component (SC) and facilitate the transport of the completed IgA molecule. It has been speculated that the accumulation of IgA plasmacytes in mucosal lamina propria and the interstitium of secretory glands is the consequence of a selective homing of IgA precursor cells from remote lymphoid tissue into secretory sites; this process may be mediated by the presence of SC on the surface of exocrine epithelial cells that attracts lymphoblasts bearing SC receptors (1–3). This contention is supported by observations of the lack of IgA cells in the exocrine lamina propria of an SC-deficient patient (4), and the detection of SC receptors on the surface of porcine lymphocytes (5).

Keywords

Peripheral Blood Lymphocyte Lymphoblastoid Cell Line Human Peripheral Blood Lymphocyte Secretory Component Mucosal Lamina Propria 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. 1.
    Brandtzaeg, P., Nature New Biol. 243: 142, 1973.PubMedGoogle Scholar
  2. 2.
    Guy-Grand, D., Griscelli, C. and Vassalli, P., Adv. Exp. Med. Biol. 45: 41, 1974.PubMedGoogle Scholar
  3. 3.
    Williams, A. F. and Gowans, J. L., J. Exp. Med. 141: 335, 1975.PubMedCrossRefGoogle Scholar
  4. 4.
    Strober, W., Krakauer, R., Klaeveman, H. L., Reynolds, H. V. and Nelson, D. L., New Engl. J. Med. 294: 351, 1976.PubMedCrossRefGoogle Scholar
  5. 5.
    Setcavage, T. M., Rothlein, R., Muscoplat, C. and Kim, Y. B., Cell. Immunol. 27 47, 1976.CrossRefGoogle Scholar
  6. 6.
    Mach, J. P., Nature 228: 1278, 1970.PubMedCrossRefGoogle Scholar
  7. 7.
    Radl, J., Klein, F., van den Berg, P., de Bruyn, R. M. and Hijmans, W., Immunology 20: 843, 1971.PubMedGoogle Scholar
  8. 8.
    Brandtzaeg, P., Adv. Exp. Med. Biol. 45: 87, 1974.PubMedGoogle Scholar
  9. 9.
    Huang, S. W., Fogh, J. and Hong, R., Scand. J. Immunol. 5: 263, 1976.PubMedCrossRefGoogle Scholar
  10. 10.
    Mestecky, J., Kulhavy, R. and Kraus, F. W., J. Immunol. 108: 738, 1972.PubMedGoogle Scholar
  11. 11.
    Schrohenloher, R. E. and Mestecky, J., J. Immunol. 111: 1699, 1973.PubMedGoogle Scholar
  12. 12.
    Brandtzaeg, P., Scand. J. Immunol. 3: 579, 1974.PubMedCrossRefGoogle Scholar
  13. 13.
    Winchester, R. J., Spivn in In Vitro Methods in Cell-Mediated and Tumor Immunity (Edited by Bloom, B. R. and David, J. R.), Academic Press, Inc., New York, 1976.Google Scholar
  14. 14.
    Brandtzaeg, P., Clin. Exp. Immunol. 25: 50, 1976.PubMedGoogle Scholar
  15. 15.
    McKenna, G., personal communication.Google Scholar
  16. 16.
    Heremans, J. F., Spivn in The Antigens (Edited by Sela, M.), Vol. 2, p. 365, Academic Press, New York, 1974.Google Scholar
  17. 17.
    Brandtzaeg, P., Histochem. J. 9: 553, 1977.PubMedCrossRefGoogle Scholar

Copyright information

© Plenum Press, New York 1978

Authors and Affiliations

  • S. S. Crago
    • 1
  • S. J. Prince
    • 1
  • R. Kulhavy
    • 1
  • J. Mestecky
    • 1
  1. 1.Department of Microbiology and Institute of Dental ResearchUniversity of Alabama in BirminghamBirminghamUSA

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