Functional and phenotypic alterations in T cell subsets during the course of MAIDS, a murine retrovirus-induced immunodeficiency syndrome. 1989

H C Morse, and R A Yetter, and C S Via, and R R Hardy, and A Cerny, and K Hayakawa, and A W Hugin, and M W Miller, and K L Holmes, and G M Shearer
Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892.

The functional and phenotypic characteristics of Ly-4(CD4)+ and Ly-2(CD8)+ T cells were studied after induction of murine AIDS with LP-BM5 murine leukemia virus. Assays of spleen cells for their ability to generate in vitro CTL responses to TNP-modified autologous cells (self + x CTL) and to alloantigens (allo CTL) showed that self + x CTL responses were greatly impaired at 3 to 4 wk postinfection and were undetectable thereafter. Allo CTL responses were normal at 3 to 4 wk, but were reduced at 8 to 9 wk and absent at 14 wk postinfection. This sequential loss of self + x and allo CTL responses was related to a selective defect in Ly-4(CD4)+ Th cell function associated with impaired production of IL-2 and deficient proliferative responses to Con A or to soluble Ag. Changes in the functional characteristics of Ly-4(CD4)+ T cells were unrelated to changes in their frequency in spleen, but did correlate with marked alterations in their distribution among four subsets defined by mAb SM3C11 and SM6C10. Assays of CTL responses generated by mixtures of spleen cells from normal and infected mice suggested that active suppression of Ly-4(CD4)+ Th function may contribute to this defect. Studies of Ly-2(CD8)+ T cells showed that infection with LP-BM5 murine leukemia virus also induced a major phenotypic shift in subpopulations defined by their reactivity with mAb 6C10. However, this phenotypic change did not appear to correlate with major functional defects.

UI MeSH Term Description Entries
D007153 Immunologic Deficiency Syndromes Syndromes in which there is a deficiency or defect in the mechanisms of immunity, either cellular or humoral. Antibody Deficiency Syndrome,Deficiency Syndrome, Immunologic,Deficiency Syndromes, Antibody,Deficiency Syndromes, Immunologic,Immunologic Deficiency Syndrome,Immunological Deficiency Syndromes,Antibody Deficiency Syndromes,Deficiency Syndrome, Antibody,Deficiency Syndrome, Immunological,Deficiency Syndromes, Immunological,Immunological Deficiency Syndrome,Syndrome, Antibody Deficiency,Syndrome, Immunologic Deficiency,Syndrome, Immunological Deficiency,Syndromes, Antibody Deficiency,Syndromes, Immunologic Deficiency,Syndromes, Immunological Deficiency
D007165 Immunosuppression Therapy Deliberate prevention or diminution of the host's immune response. It may be nonspecific as in the administration of immunosuppressive agents (drugs or radiation) or by lymphocyte depletion or may be specific as in desensitization or the simultaneous administration of antigen and immunosuppressive drugs. Antirejection Therapy,Immunosuppression,Immunosuppressive Therapy,Anti-Rejection Therapy,Therapy, Anti-Rejection,Therapy, Antirejection,Anti Rejection Therapy,Anti-Rejection Therapies,Antirejection Therapies,Immunosuppression Therapies,Immunosuppressions,Immunosuppressive Therapies,Therapies, Immunosuppression,Therapies, Immunosuppressive,Therapy, Immunosuppression,Therapy, Immunosuppressive
D007376 Interleukin-2 A soluble substance elaborated by antigen- or mitogen-stimulated T-LYMPHOCYTES which induces DNA synthesis in naive lymphocytes. IL-2,Lymphocyte Mitogenic Factor,T-Cell Growth Factor,TCGF,IL2,Interleukin II,Interleukine 2,RU 49637,RU-49637,Ro-23-6019,Ro-236019,T-Cell Stimulating Factor,Thymocyte Stimulating Factor,Interleukin 2,Mitogenic Factor, Lymphocyte,RU49637,Ro 23 6019,Ro 236019,Ro236019,T Cell Growth Factor,T Cell Stimulating Factor
D007519 Isoantigens Antigens that exist in alternative (allelic) forms in a single species. When an isoantigen is encountered by species members who lack it, an immune response is induced. Typical isoantigens are the BLOOD GROUP ANTIGENS. Alloantigens,Alloantigen,Isoantigen
D007942 Leukemia, Experimental Leukemia induced experimentally in animals by exposure to leukemogenic agents, such as VIRUSES; RADIATION; or by TRANSPLANTATION of leukemic tissues. Experimental Leukemia,Experimental Leukemias,Leukemia Model, Animal,Leukemias, Experimental,Animal Leukemia Model,Animal Leukemia Models,Leukemia Models, Animal
D008809 Mice, Inbred C3H An inbred strain of mouse that is used as a general purpose strain in a wide variety of RESEARCH areas including CANCER; INFECTIOUS DISEASES; sensorineural, and cardiovascular biology research. Mice, C3H,Mouse, C3H,Mouse, Inbred C3H,C3H Mice,C3H Mice, Inbred,C3H Mouse,C3H Mouse, Inbred,Inbred C3H Mice,Inbred C3H Mouse
D008810 Mice, Inbred C57BL One of the first INBRED MOUSE STRAINS to be sequenced. This strain is commonly used as genetic background for transgenic mouse models. Refractory to many tumors, this strain is also preferred model for studying role of genetic variations in development of diseases. Mice, C57BL,Mouse, C57BL,Mouse, Inbred C57BL,C57BL Mice,C57BL Mice, Inbred,C57BL Mouse,C57BL Mouse, Inbred,Inbred C57BL Mice,Inbred C57BL Mouse
D008908 Mink Cell Focus-Inducing Viruses Strains of MURINE LEUKEMIA VIRUS discovered in 1976 by Hartley, Wolford, Old, and Rowe and so named because the viruses originally isolated had the capacity to transform cell foci in mink cell cultures. MCF viruses are generated by recombination with ecotropic murine leukemia viruses including AKR, Friend, Moloney, and Rauscher, causing ERYTHROLEUKEMIA and severe anemia in mice. MCF Viruses,Mink cell focus-inducing virus,MCF Virus,Mink Cell Focus Inducing Viruses,Mink cell focus inducing virus,Virus, MCF,Viruses, MCF
D009052 Leukemia Virus, Murine Species of GAMMARETROVIRUS, containing many well-defined strains, producing leukemia in mice. Disease is commonly induced by injecting filtrates of propagable tumors into newborn mice. Graffi Virus,Graffi's Chloroleukemic Strain,Leukemia Viruses, Murine,Mouse Leukemia Viruses,Murine Leukemia Virus,Murine Leukemia Viruses,Graffi Chloroleukemic Strain,Graffis Chloroleukemic Strain,Leukemia Viruses, Mouse
D010641 Phenotype The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment. Phenotypes

Related Publications

H C Morse, and R A Yetter, and C S Via, and R R Hardy, and A Cerny, and K Hayakawa, and A W Hugin, and M W Miller, and K L Holmes, and G M Shearer
March 1993, Clinical and experimental immunology,
H C Morse, and R A Yetter, and C S Via, and R R Hardy, and A Cerny, and K Hayakawa, and A W Hugin, and M W Miller, and K L Holmes, and G M Shearer
October 1994, European journal of immunology,
H C Morse, and R A Yetter, and C S Via, and R R Hardy, and A Cerny, and K Hayakawa, and A W Hugin, and M W Miller, and K L Holmes, and G M Shearer
July 1995, Pathology, research and practice,
H C Morse, and R A Yetter, and C S Via, and R R Hardy, and A Cerny, and K Hayakawa, and A W Hugin, and M W Miller, and K L Holmes, and G M Shearer
February 1994, Scandinavian journal of immunology,
H C Morse, and R A Yetter, and C S Via, and R R Hardy, and A Cerny, and K Hayakawa, and A W Hugin, and M W Miller, and K L Holmes, and G M Shearer
December 1990, European journal of immunology,
H C Morse, and R A Yetter, and C S Via, and R R Hardy, and A Cerny, and K Hayakawa, and A W Hugin, and M W Miller, and K L Holmes, and G M Shearer
January 1995, Springer seminars in immunopathology,
H C Morse, and R A Yetter, and C S Via, and R R Hardy, and A Cerny, and K Hayakawa, and A W Hugin, and M W Miller, and K L Holmes, and G M Shearer
December 1996, Immunology,
H C Morse, and R A Yetter, and C S Via, and R R Hardy, and A Cerny, and K Hayakawa, and A W Hugin, and M W Miller, and K L Holmes, and G M Shearer
January 1992, Archives of dermatological research,
H C Morse, and R A Yetter, and C S Via, and R R Hardy, and A Cerny, and K Hayakawa, and A W Hugin, and M W Miller, and K L Holmes, and G M Shearer
October 1993, Science (New York, N.Y.),
H C Morse, and R A Yetter, and C S Via, and R R Hardy, and A Cerny, and K Hayakawa, and A W Hugin, and M W Miller, and K L Holmes, and G M Shearer
December 1996, Clinical immunology and immunopathology,
Copied contents to your clipboard!