Stimulation of T Lymphocytes by Autologous non‐T Lymphoid Cells. Participation of HLA‐D?

Bergholtz, B. O.; Albrechtsen, D; Thorsby, E.

doi:10.1111/j.1399-0039.1977.tb00748.x

Cited by 43 publications

(1 citation statement)

References 17 publications

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“…Several authors have presented evidence supporting these findings: first, the determinants on non-T lymphoid cells stimulating autologous T cells were found to be inhibitable by anti-D immune sera (Bergholtz et al 1977); secondly, at the clonal level, a role for genes more closely linked to the HLA-DR than to the HLA-A or B locus in autoreactivity has been suggested (Hausman & Stobo 1979); finally, in a recent study, donor anti-donor autoreactivity has been shown to be inhibitable by HLA-DR and DQ, but not DP specific MoAbs in vztro following HLA-haploidentical bone marrow transplantation for severe combined immunodeficiency (De Villartay et al 1986, Fischer, personal communication).…”

Section: Discussionsupporting

confidence: 64%

MHC class II restricted self‐recognition after allostimulation: clonal analysis

et al. 1987

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After allostimulation in vitro using a combination of HLA‐A, B, C, DR, DQ, D identical but HLA‐DP different homozygous typing cells, 34 T cell clones were derived. Thirty‐one of them were alloreactive clones, but three clones were found to be autoreactive. One of these autoreactive clones was further expanded. In order to characterize in more detail the determinant restricting the autologous response, a panel of HLA‐typed peripheral blood mononuclear cells (PBMC) or Epstein‐Barr virus lymphoblastoid cell lines (EVB‐LCL) was typed. A good correlation of typing responses with the self haplotype HLA‐A1, B8, Cw7, DR3, DRw52, DQw2 was found. Typing responses also segregated together with this haplotype in informative families. Blocking studies using MHC class I and II specific monoclonal antibodies (MoAb) linked the restricting determinant to MHC class II molecules. The clone which was both autoproliferative and autocytotoxic bore the CD3(+), CD4(+), CD8(‐), Ia(+) phenotype. Antibiotics or foreign plasma proteins were ruled out as restricted determinants.

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Section: Discussionsupporting

confidence: 64%

MHC class II restricted self‐recognition after allostimulation: clonal analysis

et al. 1987

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Function of lymphocyte subpopulations in chronic lymphocytic leukemia. Activity in the allogeneic and autologous mixed lymphocyte reaction

Wolos

Davey

1980

Cancer

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Lymphocyte subpopulations from patients with chronic lymphocytic leukemia (CLL) and from normal age-matched controls were evaluated for their ability to participate in allogeneic and autologous mixed lymphocyte reactions (MLR). Unfractionated and T enriched lymphocyte populations from normal age-matched controls responded well to allogeneic stimulation. T enriched lymphocytes from patients will CLL also responded to allogeneic lymphocytes. B enriched lymphocytes from normal age-matched individuals produced a stronger stimulus in the allogeneic MLR than did unfractionated mononuclear cell populations. Unfractionated and B enriched lymphocyte subpopulations from patients with CLL were poor stimulators in the allogeneic MLR. In normal age-matched controls T enriched lymphocyte subpopulations were able to respond to autologous B enriched lymphocytes. Autologous mixed lymphocyte cultures from patients with CLL failed to demonstrate any activity.

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Diminished autologous mixed lymphocyte reaction in patients with hodgkin disease: Evidence for non‐t cell dysfunction

et al. 1982

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In the autologous mixed lymphocyte reaction (AMLR), T lymphocytes are stimulated to proliferate by autologous non-T mononuclear cells. In five untreated patients with Hodgkin disease, the AMLR was diminished. In addition, in the same five patients, T cell response PHA was inhibited by a cell in the non-T cell fraction, the response of non-T cells to PWM was diminished, and there was a diminished ability of the non-T cell population to stimulate in allogeneic MLR. However, the response of T cells from patients with Hodgkin disease to allogeneic antigen was normal. The AMLR and allogeneic MLR were then studied in an additional five untreated patients before and after monocyte depletion of the stimulating non-T mononuclear cell population. In this second group of Hodgkin disease patients, the AMLR was again diminished when T cells were incubated either with non-T cells or non-T cells depleted of monocytes. In the Hodgkin patients, monocyte depletion did not alter the T cell response in the AMLR. In the controls, monocyte depletion greatly diminished the proliferative response. The diminished AMLR in untreated Hodgkin disease patients may be the result of a failure of adequate monocyte stimulation of autologous T cells.

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Stimulation of T Lymphocytes by Autologous non‐T Lymphoid Cells. Participation of HLA‐D?

Cited by 43 publications

References 17 publications

MHC class II restricted self‐recognition after allostimulation: clonal analysis

MHC class II restricted self‐recognition after allostimulation: clonal analysis

Function of lymphocyte subpopulations in chronic lymphocytic leukemia. Activity in the allogeneic and autologous mixed lymphocyte reaction

Diminished autologous mixed lymphocyte reaction in patients with hodgkin disease: Evidence for non‐t cell dysfunction

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