       Document 0201
 DOCN  M9580201
 TI    CD4+ T lymphocyte infiltration correlates with regression of a
       UV-induced squamous cell carcinoma.
 DT    9506
 AU    Patel A; Halliday GM; Barnetson RS; Department of Dermatology,
       University of Sydney, Royal Prince; Alfred Hospital, Australia.
 SO    J Dermatol Sci. 1995 Jan;9(1):12-9. Unique Identifier : AIDSLINE
       MED/95244405
 AB    It is currently unknown which arm of the immune system is responsible
       for regression of tumours. We have studied the T lymphocytes
       infiltrating a spontaneously regressing murine squamous cell carcinoma
       during the growth, plateau and regression phases of tumour development.
       In the plateau phase, where tumour growth is partially controlled by the
       immune system so that tumour size remains static, there was a
       considerable influx of CD4+ cells into the tumour. There was also an
       increase in the number of cells expressing the receptor for interleukin
       2 (IL-2R), indicating that these cells were probably activated. The
       number of CD4+ cells remained high during the regression phase, where
       immunological destruction exceeded tumour growth. In contrast, CD8+
       cells were only present in low numbers, and did not change during growth
       or regression of the tumours. These results indicate that CD4+ cells are
       probably responsible for tumour destruction. Thus CD4+ T lymphocytes are
       able to mediate tumour rejection and should be given more consideration
       for immunotherapy.
 DE    Animal  Carcinoma, Squamous Cell/ETIOLOGY/*IMMUNOLOGY/PATHOLOGY
       CD4-Positive T-Lymphocytes/*IMMUNOLOGY/PATHOLOGY  CD8-Positive
       T-Lymphocytes/IMMUNOLOGY/PATHOLOGY  Female  Lymphocyte Count  Mice
       Mice, Inbred HRS  Neoplasm Regression, Spontaneous/*IMMUNOLOGY/PATHOLOGY
       Receptors, Interleukin-2/METABOLISM  Skin
       Neoplasms/ETIOLOGY/*IMMUNOLOGY/PATHOLOGY  T-Lymphocyte
       Subsets/IMMUNOLOGY/PATHOLOGY  Time Factors  Ultraviolet Rays/ADVERSE
       EFFECTS  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

