Old mice express a transient early resistance to pulmonary tuberculosis that is mediated by CD8 T cells.
During the natural aging process the immune system undergoes many alterations. In particular, both the CD4 and CD8 T-cell compartments become compromised, and these changes have serious implications for the capacity of the elderly to control infection. As a result, the elderly are more susceptible to many infectious diseases, including primary infection and reactivation of latent infections. In this study we addressed the capacity of old mice to control an infection with Mycobacterium tuberculosis and to characterize the mechanism by which old mice, paradoxically, can express a transient early resistance to infection. This resistance was shown to be associated with the presence of CD8 T cells within the lungs that were capable of secreting gamma interferon, as illustrated by the demonstration that early resistance was lost in aged CD8 gene-disrupted mice. These studies therefore show that, despite a documented decline in general CD8 T-cell responsiveness in the elderly, a subset of CD8 T cells is an important early mediator of protection in the lungs of old mice that have been infected with M. tuberculosis.
Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins 80523, USA. Joanne.Turner@colostate.edu
Joanne
J
Turner
Anthony A
AA
Frank
Ian M
IM
Orme
D000375:Aging / Q000276:immunology*; D000818:Animals; D000941:Antigens / Q000096:biosynthesis / Q000276:immunology; D000950:Antigens, Ly; D000954:Antigens, Surface; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D016827:CD8 Antigens / Q000235:genetics / Q000276:immunology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology*; D004195:Disease Models, Animal; D005260:Female; D018390:Gene Targeting; D018960:Hyaluronan Receptors / Q000096:biosynthesis / Q000276:immunology; D007113:Immunity, Innate / Q000276:immunology; D007371:Interferon-gamma / Q000096:biosynthesis; D007694:Killer Cells, Natural / Q000276:immunology; D037181:Lectins, C-Type; D008168:Lung / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D008562:Membrane Glycoproteins / Q000096:biosynthesis / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D009169:Mycobacterium tuberculosis / Q000254:growth & development / Q000276:immunology*; D055651:NK Cell Lectin-Like Receptor Subfamily B; D014176:Protein Biosynthesis; D011506:Proteins / Q000276:immunology; D017452:Receptors, IgG / Q000096:biosynthesis / Q000276:immunology; D011971:Receptors, Immunologic / Q000096:biosynthesis / Q000276:immunology; D015375:Receptors, Interleukin-2 / Q000096:biosynthesis / Q000276:immunology; D055630:Receptors, NK Cell Lectin-Like; D055607:Receptors, Natural Killer Cell; D016176:T-Lymphocyte Subsets / Q000276:immunology; D014397:Tuberculosis, Pulmonary / Q000276:immunology*
D000941:Antigens; D000950:Antigens, Ly; D000954:Antigens, Surface; D016827:CD8 Antigens; D018960:Hyaluronan Receptors; D037181:Lectins, C-Type; D008562:Membrane Glycoproteins; D055651:NK Cell Lectin-Like Receptor Subfamily B; D011506:Proteins; D017452:Receptors, IgG; D011971:Receptors, Immunologic; D015375:Receptors, Interleukin-2; D055630:Receptors, NK Cell Lectin-Like; D055607:Receptors, Natural Killer Cell; D007371:Interferon-gamma