Immunologic Responses of the Autochthonous Host against Tumors Induced by Ultraviolet Light
Skin cancer can be induced in mice by exposing them repeatedly to ultraviolet (UV) light over a long period of time. Recently, we reported that tumors with spindle cell morphology, induced in inbred mice by chronic UV irradiation, are highly antigenic and have individual or non–crossreacting, tumor specific transplantation antigens (1). Most tumors of this type are immunologically rejected after transplantation to normal syngeneic recipients and grow only in immunologically deficient hosts. In spite of their strong antigenicity, these tumors grow progressively in the primary host and rarely undergo regression in situ. Thus, the animal in which the tumor has arisen is incapable of mounting an effective immunologic attack against the developing tumor, even though a normal syngeneic recipient will reject the tumor after primary transplantation. This suggests that mechanisms exist that enable these tumors to escape immunologic destruction in situ, and/or that the immune response of the primary host is altered in a way that favors, rather than hinders, tumor growth. Here, we address the following question: Why does the primary host fail to reject its own highly antigenic tumor?
KeywordsPrimary Host Syngeneic Host Spindle Cell Morphology Strong Antigenicity Tumor Allograft
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- 5.Kripke, M.L., Gruys, M.E., and J.B. Hibbs, Jr. Submitted for publicationGoogle Scholar