title: T cell deletion induced by chronic infection with mouse mammary tumor virus spares a CD25-positive, IL-10-producing T cell population with infectious capacity.
abstract: We found that T cells recognizing viral superantigen (vSAG) can be subdivided into two distinct functional subsets based on IL-2R alpha (CD25) expression. CD4+Vbeta6+CD25- and CD4+Vbeta6+CD25+ T cells were sensitive to vSAG activation. When obtained from BALB/c(SW) mice, both subsets were infected and capable to induce the tolerance process when transferred into noninfected recipients. However, in contrast to CD4+Vbeta6+CD25- cells, which were gradually deleted in MMTV(SW)-infected mice, the pool of CD4+Vbeta6+CD25+ lymphocytes was constant even at the end of the deletion process, and maintained a limited reactivity to vSAG-induced activation. The constant number of Vbeta6+CD25+ observed in infected mice could not be explained by their rapid turnover (deletion and renewal), as their proliferative rate measured by BrdU incorporation was similar in infected and naive mice, as well as in virus-nonspecific (Vbeta8.2+) cells. Neither was the Vbeta6+CD25+ subset dependent on vSAG activation since it was also present in MMTV-free mice and was not generated from Vbeta6+CD25- cells upon in vivo vSAG stimulation. Vbeta6+CD25+ T cells constitutively expressed IL-4 and IL-10 mRNA. IL-10 has been shown to be associated with viral, bacterial, and parasitic infections. This permanent CD25+ subpopulation may play a role in the control of viral infection and tolerance induction via vSAG recognition and IL-10 production.
authors.affiliation: INSERM Unit 345, Necker Institute, Paris, France.
authors.forename: M
authors.initials: M
authors.lastname: Papiernik
authors.lastname: do Carmo Leite-de-MoraesM
authors.forename: C
authors.initials: C
authors.lastname: Pontoux
authors.forename: A M
authors.initials: AM
authors.lastname: Joret
authors.forename: B
authors.initials: B
authors.lastname: Rocha
authors.forename: C
authors.initials: C
authors.lastname: Penit
authors.forename: M
authors.initials: M
authors.lastname: Dy
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000378:metabolism; D000945:Antigens, Differentiation, T-Lymphocyte / Q000378:metabolism; D000956:Antigens, Viral / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000166:cytology* / Q000276:immunology / Q000382:microbiology; D018414:CD8-Positive T-Lymphocytes / Q000166:cytology / Q000276:immunology; D017637:Clonal Deletion; D016207:Cytokines / Q000235:genetics; D015870:Gene Expression; D007108:Immune Tolerance; D016753:Interleukin-10 / Q000096:biosynthesis*; D037181:Lectins, C-Type; D008213:Lymphocyte Activation; D008324:Mammary Tumor Virus, Mouse / Q000276:immunology*; D051379:Mice; D008807:Mice, Inbred BALB C; D012333:RNA, Messenger / Q000235:genetics; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000235:genetics / Q000502:physiology; D015375:Receptors, Interleukin-2 / Q000032:analysis*; D012192:Retroviridae Infections / Q000276:immunology*; D018089:Superantigens / Q000276:immunology*; D016176:T-Lymphocyte Subsets / Q000166:cytology / Q000276:immunology*; D014412:Tumor Virus Infections / Q000276:immunology*; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D000956:Antigens, Viral; D016207:Cytokines; D016753:Interleukin-10; D037181:Lectins, C-Type; D012333:RNA, Messenger; D016693:Receptors, Antigen, T-Cell, alpha-beta; D015375:Receptors, Interleukin-2; D018089:Superantigens; D000099192:CD69 Antigens