Surface markers of resting and activated human T cells. Functional implications and experimental limits

Mingari, Maria Cristina; Moretta, Alessandro; Pantaleo, Giuseppe; Moretta, Lorenzo

doi:10.1007/bf01857432

Cited by 5 publications

(1 citation statement)

References 56 publications

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“…Limitations of cell surface marker approach. Some of the limitations of the use of monoclonal antibodies as cell surface markers were recently discussed by Mingari et al (1982): i. The specificity of lymphocyte reactivity is usually defined in operative terms, e.g., T-lymphocytes are commonly defined as cells which form E-rosettes, yet recent data has shown that under certain conditions some non-T-cells may also form E-rosettes (Ortaldo et al 1981).…”

Section: Monoclonal Antibodies and Graft Rejectionmentioning

confidence: 99%

Analysis of Intragraft Effector Mechanisms Associated with Human Renal Allograft Rejection: Immunohistological Studies with Monoclonal Antibodies

Hancock

1984

Immunological Reviews

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Immunohistological studies of rejecting human renal allografts show that the onset of graft rejection is accompanied by the influx of small numbers of T-cells and macrophages. Both cell types occur in focal aggregates adjacent to the Class II antigen-rich renal vasculature and glomerular Bowman's capsule. Although most of the T-cells express the OKT8+ phenotype of cytotoxic T-cells, analysis with markers for activation of T-cells suggests that the vast majority of these cells are present as functionally inactive precursor cells. Smaller numbers of OKT4+ helper T-cells, NK cells and occasional B-cells are also present. Within a few days, up to 15% of T-cells express receptors for IL-2 and other activation markers, suggesting that they are now functionally active. OKT8+ T-cells continue to predominate, but at least some OKT4+ T-cells appear active as DTH cells. A large influx of mononuclear cells, particularly macrophages, follows and these cells are found within and adjacent to the large Class I antigen-rich intertubular capillary network. Many of these intragraft macrophage express pro-coagulant function, presumably through lymphokine-induced activation, and are enmeshed in a fibrin network. Irreversible kidney damage may result from the combined onslaught of these cellular and humoral mechanisms, and examination of nephrectomy specimens suggests that this destruction is principally mediated by macrophages and polymorphs. These studies, by showing the presence of multiple functionally active cell types within rejecting grafts, provide evidence for a multiplicity of intragraft effector mechanisms. This evidence indicates that in addition to cytotoxic T-cells, DTH cells, macrophages, NK, K and B cells contribute to the rejection process. Further unravelling of the complex response and, hence, greater insights into the basis for more effective immunosuppression are likely to follow from the immunohistological application of monoclonal antibodies to rejecting grafts. However, comparison with animal models of kidney rejection already suggests that there may be important differences in both the initiation and effector phases of human kidney allograft rejection.

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Section: Monoclonal Antibodies and Graft Rejectionmentioning

confidence: 99%

Analysis of Intragraft Effector Mechanisms Associated with Human Renal Allograft Rejection: Immunohistological Studies with Monoclonal Antibodies

Hancock

1984

Immunological Reviews

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Decrease of the okt8 positive t cell subset in polymyalgia rheumatica

Benlahrache

Auquier

et al. 1983

Arthritis & Rheumatism

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Peripheral T cell populations were investigated in 35 patients suffering from polymyalgia rheumatica. The total number of T cells was low compared with those of a control group of similar age (P < 10 -?. This decrease was demonstrated by using both classic E-rosette and monoclonal antibody techniques (OKT3, and OKT4 + OKTS) and was shown to be secondary to a selective TS defect (P < There was no correlation between the decrease in T8 (a cytotoxic suppressor T cell subset) and steroid therapy, disease activity, and temporal arteritis, nor between this decrease and the T y percentage and the presence of circulating immune complexes (CIC).The T y cell percentage was low in the patient group (P < lo-') and correlated with the presence of detectable CIC (P < 0.05). In contrast to the TS and T y defects, concanavalip A-stimulated cells from 5 selected patients were found capable of suppressing in vitro anti-trinitrophenyl response. This suppression was found in both autologous and allogeneic experiments. From these data one can assume that an immune anomaly (T8 defect) could be the origin of CIC and the disease occurrence.

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Low Dose Ciclosporin (CyA) and Prednisone — a Step in the Direction of Selective Immunosuppression in Rheumatoid Arthritis Refractory to Treatment (6-Month Follow-Up)

Herzog

Groß

1985

Ciclosporin in Autoimmune Diseases

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Surface markers of resting and activated human T cells. Functional implications and experimental limits

Cited by 5 publications

References 56 publications

Analysis of Intragraft Effector Mechanisms Associated with Human Renal Allograft Rejection: Immunohistological Studies with Monoclonal Antibodies

Analysis of Intragraft Effector Mechanisms Associated with Human Renal Allograft Rejection: Immunohistological Studies with Monoclonal Antibodies

Decrease of the okt8 positive t cell subset in polymyalgia rheumatica

Low Dose Ciclosporin (CyA) and Prednisone — a Step in the Direction of Selective Immunosuppression in Rheumatoid Arthritis Refractory to Treatment (6-Month Follow-Up)

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