Publication Date:
1984-05-11
Description:
Long-term exposure of C3H mice to ultraviolet radiation resulted in the formation of suppressor T cells that recognize ultraviolet radiation-induced regressor skin cancers as a class before the appearance of overt tumors. Administration of monoclonal antibodies to the product of the I-Jk subregion of the major histocompatibility complex or low doses of cyclophosphamide in vivo inhibited the development or activity of these cells. This activity of the monoclonal antibody was eliminated by adsorption on B10.BR (I-Jk) but not B10.D2 (I-Jd) splenocytes. These findings provide evidence that elements expressing the I-J determinant are important in regulating the host response prior to the overt development of ultraviolet radiation-induced skin cancers and suggest novel therapeutic approaches to malignancies or other diseases involving suppressor T cells in their pathogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Granstein, R D -- Parrish, J A -- McAuliffe, D J -- Waltenbaugh, C -- Greene, M I -- 1F32 CA07014-102/CA/NCI NIH HHS/ -- AI 18072/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1984 May 11;224(4649):615-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6231725" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
Antibodies, Monoclonal/immunology
;
Cyclophosphamide/pharmacology
;
H-2 Antigens/immunology
;
Mice
;
Mice, Inbred C3H
;
Neoplasms, Experimental/immunology
;
Spleen/cytology
;
T-Lymphocytes, Regulatory/drug effects/*immunology/radiation effects
;
Ultraviolet Rays
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
