title: Interleukin 2 induction of proliferation in resting T lymphocytes requires contact with monocytes.
abstract: Resting human T cells are known to express significant numbers of intermediate but none or barely detectable low and high affinity IL-2 receptors (IL-2R). IL-2 alone failed to induce proliferation in these cells. However, in presence of small proportion of autologous monocytes, as low as 22 pM, IL-2 induced high levels of proliferation in resting T cells. Introduction of a semi permeable membrane between the two cell types or addition of an anti-CD11b mAb inhibited such induction of proliferation by IL-2. Neither recombinant IL-1 nor IL-1-containing cell-free extracts from activated monocytes substituted for intact monocytes. Autologous B cells failed to replace monocytes. Using antigen-specific cloned human T cells we have shown a lack of requirement for antigen. The proliferation was inhibited by anti-IL-2R alpha mAb. IL-2 appears to be unique since neither IL-4 nor IL-6, alone or in presence of monocytes, led to induction of proliferation in resting T cells. Combination of IL-2 and monocytes induced proliferation in all T cell subpopulations (CD4+, CD8+, CD45RA+ and CD45RO+) and antigen-specific clones examined. It also induces mRNA and surface expression of IL-2R alpha, appearance of high affinity IL-2R and induction of proliferation in large proportions of T cells. As in humans, the IL-2 induction of proliferation in murine resting T cells required contact with syngeneic monocytes, suggesting that such a mechanism of T cells activation is highly conserved.
authors.affiliation: Laboratorio de Inmunogenética y Diagnóstico Molecular, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Argentina.
authors.forename: S
authors.initials: S
authors.lastname: Pesoa
authors.forename: A
authors.initials: A
authors.lastname: Martín
authors.forename: A L
authors.initials: AL
authors.lastname: Mariani
authors.forename: C
authors.initials: C
authors.lastname: Vullo
authors.forename: H
authors.initials: H
authors.lastname: Serra
mesh_terms: D000818:Animals; D018929:Cell Culture Techniques; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000494:pharmacology; D007376:Interleukin-2 / Q000494:pharmacology* / Q000502:physiology; D008213:Lymphocyte Activation / Q000187:drug effects*; D051379:Mice; D008807:Mice, Inbred BALB C; D009000:Monocytes / Q000166:cytology / Q000502:physiology*; D015375:Receptors, Interleukin-2 / Q000502:physiology*; D011994:Recombinant Proteins; D013601:T-Lymphocytes / Q000187:drug effects* / Q000502:physiology; D013936:Thymidine
chemical_list: D000077190:Interferon alpha-2; D016898:Interferon-alpha; D007376:Interleukin-2; D015375:Receptors, Interleukin-2; D011994:Recombinant Proteins; D013936:Thymidine