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L Boumsell

Publications and source records attributed to L Boumsell.

143 records · Page 8Linked to original sources
PubMed1980

An antigen shared by a human T cell subset and B cell chronic lymphocytic leukemic cells. Distribution on normal and malignant lymphoid cells.

We obtained a monoclonal antibody, A50, after immunizing Biozzi's high responder strain of mice with T cell chronic lymphocytic leukemia (T-CLL) cells. A50 recognized an antigen present on the surface of B cell chronic lymphocytic leukemia cells from many patients and from cells of T lineage from any subject we tested. We could not find this antigen either on the surface of normal B cell or on other non-T cell malignancies. On T cells, this antigen was present on a subpopulation of thymus cells, and on most peripheral T cells. The antigen was present on the surface of cells from T-CLL, Sézary's disease, and a subset o T cell lymphoma. The antigen seemed to belong to a complex set of antigenic determinants that we had defined with rabbit antisera.

Animals↗
PubMed1980

High efficiency of Biozzi's high responder mouse strain in the generation of antibody secreting hybridomas.

While preparing monoclonal antibodies against human lymphocyte surface antigens, we compared two strains of mice, which had been genetically selected by Biozzi et al. (1970) for their high and low antibody responses to sheep erythrocytes. Biozzi et al. (1975) subsequently showed that these high and low responder strains (HR and LR) have a high and low antibody response to almost any antigen. We observed with the HR strain a huge increase in the number of hybrids secreting an antibody directed against human lymphocytes.

Animals↗
PubMed1979

Human T cell differentiation antigens and correlation of their expression with various markers of T cell maturation.

Two sets of differentiation antigens are demonstrated on human T cells by using 11 heterologous anti-human antisera raised against various normal and malignant T cells. The two antigenic determinants from the first set of differentiation antigens are expressed only on thymus cells and on T lymphoblasts, whereas the two antigenic determinants from the second set are expressed on blood T cells, Sezary cells, T.CLL cells, and thymus cells. Four T cell phenotypes are thus defined; two phenotypes are expressed only by T lymphoblasts, whereas the other two phenotypes are expressed both by normal and malignant T cells. Moreover, a clear-cut relationship exists between the four T cell antigenic phenotypes and two other markers of T cell differentiation: terminal deoxynucleotidyl transferase and peanut agglutinin. Two phenotypes are linked with the presence of TdT, one phenotype is linked with the affinity for PNA, and the fourth phenotype is correlated with the absence of both markers.

Acute Disease↗
PubMed1979

Subsets of malignant lymphomas in children related to the cell phenotype.

We studied the lymphomatous cells of 39 children presenting with the classical features of malignant lymphoma. Twenty-two had T lymphoblasts. We could classify these patients into three subsets: The T lymphoblasts from children group 1 displayed antigen(s) shared by a thymocyte subpopulation, had terminal deoxynucleotidyl transferase (TDT), but no affinity for peanut agglutinin (PNA). The T lymphoblasts from children group 2 lacked the thymocyte antigen(s), had no TDT, but showed affinity for PNA. The T lymphoblasts from children group 3 displayed mature T-cell antigens, had no TDT, and no affinity for PNA. Children from the three groups were similar in terms of clinical presentation, age and sex distribution, and cell morphology; however patients from the three groups might have a different prognosis. Fourteen children had B lymphoblasts that, in half of the cases, had affinity for Helix pomatia agglutinin. Three patients had lymphoblasts lacking specific marker. Two of them had cells displaying an antigen found on common acute lymphoblastic leukemia cells and had TDT.

Adolescent↗
PubMed1978

Some chronic lymphocytic leukemia cells bearing surface immunoglobulins share determinants with T cells.

One set of antigens is common to some chronic lymphocytic leukemia (CLL) cells bearing surface immunoglobulins (Ig) and normal T cells. Proliferating cells from thirty-eight patients were studied with four antisera recognizing normal human T but not B cells. These antisera were raised in rabbits against (a) Sezary cells, (b) blood lymphocytes from a patient with sex-linked agammaglobulinemia, (c) T lymphoblasts and (d) thymus cells. In four CLL cases, the cells expressed the receptor for sheep erythrocytes and lacked surface Ig. Cells from thirty-four CLL cases bore monoclonal surface Ig and did not bind sheep erythrocytes. Twelve out of these thirty-four cases of CLL had cells which were lysed by one or, more frequently, by the four anti-human T cell xenoantisera. By absorption experiments, one set of at least three antigens common to the cells of some of these CLL and T cells was defined. Depending on the patient, the cells can either carry one, some or all of the antigens of this set. However, it was also demonstrated by absorption that these cells lacked antigens particular to the T cell lineage, while the cells from T CLL cases carried both sets of antigens.

Animals↗
PubMed1976

Leukocyte-derived complement inhibitor. IV. The functional properties of C1 bound to erythrocytes pretreated with leukocyte culture supernatant.

E, pretreated with leukocyte cultures supernatant (ES), binds C1 through C1q; ES and EIgM that bind the same amount of C1 as measured in a hemolytic assay have the same uptake of 125I-C1q; ESC1q and EIgMC1q, carrying the same number of molecules of CUq per cell, have the same uptake of CUr and CUs; soluble immune compleses prevent the binding of C1 and C1q to ES. The activity of C1 bound to ES is impaired; ESC1 can react with C4 but not with C2. The C4 turnover and the C1 ING turnover by ESC1 are reduced so that ES-bound C1 is protected from destruction by C1 ING. These modifications are fully reversed when C1 is transferred from ES to EA:C1 recovers its ability to react with C2, and C1 INH. Thus the C1s activity can be modulated inside the C1 molecular complex upon binding of C1q to a lymphocyte product. In addition, the 125I-C1q uptake is proportional to the amount of IgM hemolysin used to sensitize E; it has, however, an exponential relationship to the amount of IgG or S used to sensitize E. The ratio of 125I-C1q uptake towhole C1 uptake measured in a hemolytic assay is lowerthan 2. This indicates that one molecule of IgM is sufficient to bind one molecule of C1q on E, that several molecules of IgG or S are required to bind one molecule of C1q, and that one molecule of C1q is sufficient to create a lytic site on E.

Animals↗
PubMed1975

Complement inhibitor(s) released by leukocytes. I. Pretreatment of sheep erythrocytes with supernatants of mouse spleen and thymus cells inhibit whole complement activity and C2 utilization.

Sheep erythrocytes pretreated with supernatants of mouse spleen or thymus cells become resistant to lysis by guinea pig complement. The inhibitory activity (IA) reduces the utilization of C2 by EAC14. Because IA binds to the surface of sheep erythrocytes and does not inhibit C1 irreversibly, it is probably a hitherto undescribed inhibitor of complement.

Animals↗
PubMed1975

Complement inhibitor(s) released by leukocytes. III. Evidence for a "new" C1 inhibitor in the supernatants of short-term cultures of mouse spleen and thymus cells.

Mouse spleen or thymus cells in short-term culture release a factor, designated S, that binds to sheep erythrocytes (E). Supernatant-treated sheep erythrocytes (SE) are capable of fixing and transferring the activated first component of guinea pig complement. SEC1, however is not capable of initiating hemolysis by the rest of the complement components. SE is capable of binding but not activating native C1; native C1 bound to SE seems irreversibly inhibited. Evidence is presented that S may be the same factor as the previously described inhibitor released by mouse spleen or thymus cells that inhibits the utilization of C2 by EAC14.

Animals↗
PubMed1975

Mouse mononuclear cell chemotaxis. I. Differential response of monocytes and macrophages.

The chemotactic responses of peripheral blood monocytes and peritoneal macrophages to lymphocyte- and complement-derived stimuli were studied in vitro. Monocyte and macrophage chemotactic responses to these stimuli were different in both dose-response and time course. These differences provide a useful functional marker between these two cell populations.

Animals↗
PubMedDate not supplied

[Value of immunological investigations in a difficult diagnosis of acute lymphoblastic leukaemia (author's transl)].

A 9-year-old child was found to have massive invasion of his bone marrow by malignant cells. Experienced pathologists were unable to determine on morphological grounds the nature of these cells, even after electron microscope study and multiple cytochemical staining of bone marrow smears. However, serological analysis of the cells showed that they displayed an antigen specific to cells from common acute lymphoblastic leukaemia HLA-DR antigens and contained high concentrations of terminal deoxynucleotidyl transferase. A course of the chemotherapy usually prescribed for common acute lymphoblastic leukaemia resulted in complete remission.

Child↗
PubMedDate not supplied

[Search for antilymphocytic antibodies in the serum of 67 children with juvenile chronic arthritis].

We sought the presence of lymphocytotoxic antibodies in the serum of 67 children with juvenile rheumatoid arthritis. We demonstrated in the serum of a large number of children (more than 50 %) antibodies reacting mainly with the cells not forming spontaneously rosettes with sheep red cells and/or all the mononuclear cells of the peripheral blood of normal subjects. These antibodies which are more active at 4 degrees C than at 20 degrees C are absorbable on red cells, and/or the platelet pool and present the characteristics of cold lymphocytotoxins. The presence of these antibodies was not correlated with either the clinical form of juvenile rheumatoid arthritis, nor with the duration of the course, nor with the treatment. Generally speaking, such antibodies are found during diseases where regulation of the immune response is modified.

Adolescent↗