Chapter 15. The Biological Basis of Immunosuppression

  1. Ruth Porter and
  2. Julie Knight
  1. M. C. Berenbaum

Published Online: 30 MAY 2008

DOI: 10.1002/9780470719985.ch15

Ciba Foundation Symposium 15 - Corneal Graft Failure

Ciba Foundation Symposium 15 - Corneal Graft Failure

How to Cite

Berenbaum, M. C. (1973) The Biological Basis of Immunosuppression, in Ciba Foundation Symposium 15 - Corneal Graft Failure (eds R. Porter and J. Knight), John Wiley & Sons, Ltd, Chichester, UK. doi: 10.1002/9780470719985.ch15

Author Information

  1. Wellcome Laboratories of Experimental Pathology, St Mary's Hospital Medical School, London

Publication History

  1. Published Online: 30 MAY 2008
  2. Published Print: 1 JAN 1973

ISBN Information

Print ISBN: 9789021940168

Online ISBN: 9780470719985



  • immunosuppression;
  • haemolytic disease;
  • corticosteroids;
  • x-irradiation;
  • alkylating agents


The various mechanisms involved in specific immune responses are: (1) antigen recognition, (2) cell cooperation, (3) cell traffic, (4) cell proliferation, and (5) differentiation and function. In addition: (6) non-specific immune mechanisms almost invariably accompany specific immune responses in vivo.

Immunosuppressive agents can interfere with each of these mechanisms. (1) Antigen recognition can be blocked by administration of antibody (as in the prevention of haemolytic disease of the newborn).

(2) Cell cooperation can be prevented by damaging one of the cooperating cell populations (e.g. antilymphocyte serum preferentially damages recirculating long-lived lymphocytes, the cooperation of which is necessary in the antibody response to certain antigens).

(3) Lymphocyte traffic is impeded by corticosteroids.

(4) Cell proliferation can be prevented by antimetabolites (azathioprine, 6-mercaptopurine, methotrexate, etc.) which inhibit enzymes used in nucleic acid synthesis, and by X-irradiation and alkylating agents (cyclophosphamide, chlorambucil, etc.) which damage nucleic acid templates.

(5) Cell differentiation and function can, in theory, be interfered with by drugs that inhibit synthesis of RNA or protein (actinomycin, chloramphenicol), but these agents are probably immunosuppressive by virtue of their ability to prevent cell proliferation.

(6) Non-specific immunity (epithelial integrity, phagocytosis, inflammatory response. interferon, complement, etc.) is impaired by most immunosuppressive agents and these effects may be as important clinically as suppression of specific immunity.

In addition, many agents cause outright destruction of lymphocytes (X-rays, alkylating agents, corticosteroids, asparaginase) but the role of this in immunosuppression is not known.