Role for elevated H-2 antigen expression in resistance to neoplasia caused by radiation-induced leukemia virus. Enhancement of effective tumor surveillance by killer lymphocytes

Journal Article · Sun Apr 01 04:00:00 EST 1979 · J. Exp. Med.; (United States)

DOI:https://doi.org/10.1084/jem.149.4.898· OSTI ID:6700931

Meruelo, D

Resistance to neoplasia caused by radiation-induced leukemia virus (RadLV) is mediated by gene(s) in the H-2D region of the major histocompatibility complex. The previous observation that rapid increases in cellular synthesis and cell-surface expression of H-2 antigens are detectable immediately after virus inoculation has suggested that altered expression of H-2 antigens may play a significant role in the mechanism(s) of host defense to virus infection. This concept is supported by the following observations. First, cell-mediated immunity against RadLV transformed or infected cells can be detected with ease when H-2-positive target cells are used in the cell-mediated lympholysis (CML) assay. Second, resistant mice develop greater numbers of effectors when infected with RadLV than do susceptible mice. Third, injection of normal (uninfected) thymocytes into syngeneic recipients of resistant or susceptible H-2 type does not stimulate a CML response. However, injection of RadLV infected thymocytes from resistant mice produces a vigorous CMI response, and such thymocytes elicit the strongest response at a time when both H-2 and viral antigen expression is elevated. By contrast, injection of infected thymocytes from susceptible mice, which express viral antigens, but low levels of H-2 antigens, does not stimulate a CML reaction. These findings may explain the easier induction of leukemia found by many investigators when virus is inoculated into neonatal mice and the preferential thymus tropism of some oncogenic type-C RNA virus. Cells expressing very low levels of H-2, such as thymocytes, may serve as permissive targets for virus infection because they lack an important component (H-2 antigens) of the dual or altered recognition signal required to trigger a defensive host immune response.

• Research Organization: New York Univ., NY
• OSTI ID: 6700931
• Journal Information: J. Exp. Med.; (United States), Journal Name: J. Exp. Med.; (United States) Vol. 149:4; ISSN JEMEA
• Country of Publication: United States
• Language: English

Related Subjects

550700 -- Microbiology
551000 -- Physiological Systems
560131* -- Radiation Effects on Microorganisms-- Basic Studies-- (-1987)
59 BASIC BIOLOGICAL SCIENCES
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.
ANIMAL CELLS
ANIMALS
ANTIGENS
BIOLOGICAL MATERIALS
BIOLOGICAL RECOVERY
BIOLOGICAL REPAIR
BLOOD
BLOOD CELLS
BODY FLUIDS
CELL PROLIFERATION
CONNECTIVE TISSUE CELLS
DISEASES
GENES
HEMIC DISEASES
HOST-CELL REACTIVATION
IMMUNE REACTIONS
IMMUNITY
INFECTIVITY
LEUKEMIA
LEUKEMIA VIRUSES
LEUKOCYTES
LYMPHOCYTES
MAMMALS
MATERIALS
MICE
MICROORGANISMS
NEOPLASMS
ONCOGENIC VIRUSES
PARASITES
RADIOINDUCTION
RECOVERY
REPAIR
RODENTS
SENSITIVITY
SOMATIC CELLS
THYMOCYTES
VERTEBRATES
VIRUSES