Precursor frequency analysis of lymphokine-secreting alloreactive T lymphocytes. Dissociation of subsets producing interleukin 2, macrophage-activating factor, and granulocyte-macrophage colony-stimulating factor on the basis of Lyt-2 phenotype.

Kelso, Anne; MacDonald, H. Robson

doi:10.1084/jem.156.5.1366

Cited by 66 publications

(24 citation statements)

References 35 publications

(13 reference statements)

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“…This observation confirms and extends the findings of an earlier study of interferon, GM-CSA and &-2 production by clones classified on the basis of cytolytic phenotype (Kelso and Glasebrook, 1984) and by limiting dilution cultures of Lyt-2+ and Lyt-2-cells (Kelso and MacDonald, 1982). It also agrees with the report by Guerne et al (1984) that Lyt-2 + clones were more heterogeneous and produced lower titers of IL-2 and L-3 than Lyt-2-clones.…”

Section: Generation Of T-cell Clonessupporting

confidence: 91%

Clonal heterogeneity in colony stimulating factor production by murine T lymphocytes

Kelso

Metcalf

1985

Journal Cellular Physiology

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A panel of 55 alloreactive murine T-lymphocyte clones was screened for the production of granulocyte-macrophage colony stimulating factor (GM-CSF), multilineage CSF (multi-CSF), human-active eosinophil CSF (human-active EO-CSF), and interleukin 2 (IL-2) in response to stimulation with the lectin concanavalin A. Many clones were also characterized for cytolytic specificity and expression of the T-cell antigen receptor-associated surface markers Lyt-2 and L3T4, which reflect their specificity for Class I (H-2K, H-2D) or Class II (H-2l, Mls) histocompatibility antigens, respectively. Eighty percent of the clones secreted detectable quantities of at least one of the four factors measured. Of the factor-producing clones, all appeared to secrete GM-CSF and half also secreted multi-CSF. A subpopulation of multi-CSF producers also released human-active EO-CSF. More than half of the factor-producing clones secreted detectable IL-2; whereas the IL-2-producing clones included some that did not secrete multi-CSF, IL-2 production was always associated with concomitant synthesis of GM-CSF. Comparison of the range and quantities of factors secreted by Lyt-2+ and L3T4+ clones indicated that more L3T4+ clones produced measurable titers of the four factors; on average, this group also secreted 10- to 100-fold higher titers of both the hemopoietic regulators and IL-2 than Lyt-2+ clones. Cells of the L3T4+ phenotype would therefore be expected to account for the majority of CSF and IL-2 secretion by polyclonal populations of activated T lymphocytes.

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Section: Generation Of T-cell Clonessupporting

confidence: 91%

Clonal heterogeneity in colony stimulating factor production by murine T lymphocytes

Kelso

Metcalf

1985

Journal Cellular Physiology

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“…Concerning the cellular mechanisms of the production of MAF or IFNy, Lyt phenotypes of cells involved have been analyzed in several studies using allo antigen-or mitogen-stimulated spleen and lymph node T cells [13,15,19,25,44,47] or T cell clones in long-term cultures [3,18,29,31]. It appears from these studies that various T cell subsets are capable of producing MAF or IFNy depending on the situations such as the form of antigenic stimuli and culture periods.…”

Section: Discussionmentioning

confidence: 99%

Studies on macrophage-activating factor (MAF) in antitumor immune responses

Nakajima

Izumi

Sugihara

et al. 1987

Cancer Immunol Immunother

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In the present study we investigated some of the physicochemical properties of macrophage-activating factor(s) (MAF) produced by the tumor-immune Lyt-1+2- T cell subset. Supernatant from mixed culture of spleen and lymph node cells, obtained from C3H/HeN mice immunized with syngeneic MH134 hepatoma or MCH-1-A1 fibrosarcoma, with the corresponding tumor cells exhibited the capability of activating peritoneal exudate macrophages to exert their cytostatic and cytolytic activities on tumor cells. Such MAF production was abolished by treatment of tumor-immune spleen and lymph node cells with anti-Thy-1.2 or anti-Lyt-1.1 antibody plus complement (C) before culturing. Anti-Lyt-2.1 and/or anti-asialo GM1 plus C treatment, however, had only marginal effect on the generation of MAF by these cells, despite the complete disappearance of natural killer (NK) cell activity of spleen and lymph node cells after the treatment with anti-asialo GM1 plus C. Thus, the tumor-specific Lyt-1+2- T cell subset could fulfill a crucial role in generating MAF without the support of NK cells. The MAF activity was heat, acid, and trypsin sensitive. On Sephacryl S-300 column, MAF activity was eluated in a broad single peak around a molecular weight (m.w.) of 70,000 daltons. Antiviral activity was detected in the concentrated pool of MAF-containing fractions from Sephacryl S-300. Gel permeation analysis using HPLC also showed a coincident peak of MAF and antiviral activities at a m.w. of approximately 70,000 daltons. In addition, MAF activity was almost completely neutralized by incubation with rabbit antiserum against recombinant murine gamma-interferon (IFN gamma). Taken together, these results indicate that MAF generated by tumor-immune Lyt-1+2- T cell subset is closely related to IFN gamma.

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“…[T] + [TA] + [TA2] = Tn (5) [A] + [TA] + 2 [TA2] = An (6) where Tn is the total number of T cells per well and An is the total number of antigenic cells per well.…”

Section: (4)mentioning

confidence: 99%

“…The antigen-bearing target cell need not be metabolically active (1; 2). Cytotoxic T lymphocytes, defined either functionally or by their Lyt-2 * phenotype, can secrete lymphokines follcv^'ing antigen exposure (3)(4)(5)(6)(7). The range and amount of each lymphokine produced varies considerably between T celJs but for an individual clone it is relatively invariant following each antigen stimulation (8; 9).…”

Section: Introductionmentioning

confidence: 99%

A model of T cell‐target interaction leading to lymphokine release

McKinnon

Hodgkin

1987

Immunol Cell Biol

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Summary, Binding of antigenic cells by activated T lymphocytes can trigger the release of a number of soluble factors, including the lymphokine interleukin 3 (IL3). The cellular interactions between T cells and allogeneic cells which are involved in the triggering of lymphokine release from T cells are still poorly understood. We have examined the relationship between antigenic cell number, T cell number and IL3 release and have derived a steady state binding model which adequately accounts for the experimental data if it is assumed that triggering is an all or none phenomenon. We find that binding of at least two antigenic cells by an allo-reactive T cell is necessary to trigger lymphokine release.

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Precursor frequency analysis of lymphokine-secreting alloreactive T lymphocytes. Dissociation of subsets producing interleukin 2, macrophage-activating factor, and granulocyte-macrophage colony-stimulating factor on the basis of Lyt-2 phenotype.

Abstract: colony-stimulating factor; IL-2, interleukin 2; MAF, macrophage-activating factor; 2 ° MLC SN, secondary mixed leukocyte culture supernatant; SN, supernatant(s). 1366J. Exp. MED.

Cited by 66 publications

References 35 publications

Clonal heterogeneity in colony stimulating factor production by murine T lymphocytes

Clonal heterogeneity in colony stimulating factor production by murine T lymphocytes

Studies on macrophage-activating factor (MAF) in antitumor immune responses

A model of T cell‐target interaction leading to lymphokine release

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