The current article by Koranda et al (JAMA p 419) focuses mainly on host-defense failure and its cutaneous manifestations in transplant recipients. At most transplant centers, these patients daily receive orally administered prednisone and azathioprine to maintain their grafts. This regimen is usually administered in doses and according to a schedule that suppresses several aspects of host defense including granulocyte numbers and exudation, local mononuclear inflammatory responses, phagocytosis and intracellular killing of microorganisms, and delayed hypersensitivity as well as graft rejection.1
Thus, it is not surprising that while organ graft rejection is often prevented, host defenses (systemic as well as cutaneous) are considerably impaired, resulting in an increased incidence of wound infections, verrucae, herpes simplex, herpes zoster, tinea versicolor, and cutaneous malignant neoplasms. In each of these instances, except for bacterial infections, the main host-defense factor is cell-mediated immunity and is based on the activity of thymus-derived or "T"
Hersh EM, Freireich EJ. Focus on Cutaneous Host-Defense Failure in Transplant Recipients. JAMA. 1974;229(4):457–458. doi:10.1001/jama.1974.03230420069033
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