Cell-Interactions in the Splenic Suppression Caused by Antigen-Feeding

  • Thomas T. MacDonald
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 149)


Whereas antigen given systemically usually results in a humoral or cell-mediated immune response, antigen given by the oral route usually induces a state of tolerance (1–4). This is most often demonstrated by a reduced response to systemic antigen challenge given after the initial oral antigen administration. Several investigators have shown that the unresponsive state induced by antigen-feeding is “infectious,” that is infusion of cells from antigen-fed mice into normal recipients transfers the unresponsive state (4–6). These data would seem to indicate that antigen-feeding induces suppressor T cells, but in the light of recent findings on T cell interactions, other explanations are available; the main one of which is that antigen-feeding does not induce suppressor T cells, but instead produces “suppressor-inducers” (7, 8). These cells, when re-exposed to antigen can co-opt other T cells to become suppressor cells.


Spleen Cell Suppressor Cell Jefferson Medical College Spleen Cell Culture Normal Spleen Cell 


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  1. 1.
    M.W. Chase. Proc. Soc. Exp. Biol. Med. 61:257 (1946).PubMedGoogle Scholar
  2. 2.
    H.C. Thomas, and D.M.V. Parrott. Immunology 27:631 (1974).PubMedGoogle Scholar
  3. 3.
    C. Andre, J.F. Heremans, J.P. Vaerman, and C.L. Cambiaso. J. Exp. Med. 142:1509 (1975).PubMedCrossRefGoogle Scholar
  4. 4.
    L.K. Richman, J.M. Chiller, W.R. Brown et al. J. Immunol. 121:2429 (1978).PubMedGoogle Scholar
  5. 5.
    J. Ngan, and L.S. Kind. J. Immunol. 120:861 (1978).PubMedGoogle Scholar
  6. 6.
    S.D. Miller, and D.G. Hanson. J. Immunol. 123:2344 (1979).PubMedGoogle Scholar
  7. 7.
    D.D. Eardley, J. Hugenbeger, L. McVay-Boudreau et al. J. Exp. Med. 147:1106 (1978).PubMedCrossRefGoogle Scholar
  8. 8.
    H. Cantor, J. Hugenbeger, L. McVay-Boudreau et al. J. Exp. Med. 148:871 (1978).PubMedCrossRefGoogle Scholar
  9. 9.
    R.I. Mishell, and R.W. Dutton. J. Exp. Med. 126:423 (1967).PubMedCrossRefGoogle Scholar
  10. 10.
    M.H. Julius, E. Simpson, and L.A. Herzenberg. Eur. J. Immunol. 3:645 (1973).PubMedCrossRefGoogle Scholar
  11. 11.
    D.D. Eardley, J. Kemp, F.W. Shen et al. J. Immunol. 122:1663 (1979).PubMedGoogle Scholar
  12. 12.
    M.F. Kagnoff. Cell Immunol. 40:186 (1978).PubMedCrossRefGoogle Scholar
  13. 13.
    J.A. Mattingly, and B.H. Waksman. J. Immunol. 121:1878 (1978).PubMedGoogle Scholar
  14. 14.
    M.F. Kagnoff. J. Exp. Med. 142:1425 (1975).PubMedCrossRefGoogle Scholar
  15. 15.
    M. Hoffmann, and J.W. Kappler. J. Exp. Med. 137:721 (1973).PubMedCrossRefGoogle Scholar
  16. 16.
    J.A. Mattingly, J.M. Kaplan, and C.A. Janeway. J. Exp. Med. 152:541 (1980).CrossRefGoogle Scholar

Copyright information

© Plenum Press, New York 1982

Authors and Affiliations

  • Thomas T. MacDonald
    • 1
  1. 1.Department of MicrobiologyJefferson Medical CollegePhiladelphiaUSA

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