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Results for “Lymphocyte Cooperation”

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At least 55 records · Page 3Linked to original sources
PubMed1989

Oncogene cooperation in lymphocyte transformation: malignant conversion of E mu-myc transgenic pre-B cells in vitro is enhanced by v-H-ras or v-raf but not v-abl.

Although transgenic mice bearing a c-myc gene controlled by the immunoglobulin heavy-chain enhancer (E mu) eventually develop B-lymphoid tumors, B-lineage cells from preneoplastic bone marrow express the transgene but do not grow autonomously or produce tumors in mice. To determine whether other oncogenes can cooperate with myc to transform B-lineage cells, we compared the in vitro growth and tumorigenicity of normal and E mu-myc bone marrow cells infected with retroviruses bearing the v-H-ras, v-raf, or v-abl oncogene. The v-H-ras and v-raf viruses both generated a rapid polyclonal expansion of E mu-myc pre-B bone marrow cells in liquid culture and 10- to 100-fold more pre-B lymphoid colonies than normal in soft agar. The infected transgenic cells were autonomous, cloned efficiently in agar, and grew as tumors in nude mice. While many pre-B cells from normal marrow could also be induced to proliferate by the v-raf virus, these cells required a stromal feeder layer, did not clone in agar, and were not malignant. Most normal cells stimulated to grow by v-H-ras also cloned poorly in agar, and only rare cells were tumorigenic. With the v-abl virus, no more cells were transformed from E mu-myc than normal marrow and the proportion of tumorigenic pre-B clones was not elevated. These results suggest that both v-H-ras and v-raf, but apparently not v-abl, collaborate with constitutive myc expression to promote autonomous proliferation and tumorigenicity of pre-B lymphoid cells.

Animals↗
PubMed1989

Leukocyte function in Pelger-Huët anomaly of dogs.

Leukocyte function was evaluated in five dogs with Pelger-Huët (P-H) anomaly and in five control dogs. No significant differences were found between groups in neutrophil adherence, random movement, chemotaxis, phagocytosis, or bacterial killing of Staphylococcus intermedius. Neutrophils migrated rapidly into inflammatory sites where progressive nuclear lobulation was noted over time. Antibody titers to exogenous antigens were similar in the P-H and control groups indicating B- and T-lymphocyte cooperation in humoral immunity. Lymphocyte blastogenesis to phytohemagglutinin also was similar in both groups suggesting the presence of a responsive T-lymphocyte population. These findings indicate that no apparent predisposition to infection or immunodeficiency exists in dogs with P-H anomaly.

Animals↗
PubMed2005

N-acetylglucosamine-6-O-sulfotransferases 1 and 2 cooperatively control lymphocyte homing through L-selectin ligand biosynthesis in high endothelial venules.

Lymphocyte homing is mediated by specific interactions between L-selectin on lymphocytes and sulfated carbohydrates restricted to high endothelial venules in lymph nodes. Here we generated mice deficient in both N-acetylglucosamine-6-O-sulfotransferase 1 (GlcNAc6ST-1) and GlcNAc6ST-2 and found that mutant mice had approximately 75% less homing of lymphocytes to the peripheral lymph nodes than did wild-type mice. Consequently, these mice had lower contact hypersensitivity responses than those of wild-type mice. Carbohydrate structural analysis showed that 6-sulfo sialyl Lewis X, a dominant ligand for L-selectin, was almost completely absent from the high endothelial venules of these mutant mice, whereas the amount of unsulfated sialyl Lewis X was much greater. These results demonstrate the essential function of GlcNAc6ST-1 and GlcNAc6ST-2 in L-selectin ligand biosynthesis in high endothelial venules and their importance in immune surveillance.

Animals↗
PubMed1979

Cellular cooperation in lymphocyte activation. III. B-cell helper effect in the enhancement of T-cell response.

T and B cells were purified from human tonsil and peripheral blood by the removal of phagocytic cells, followed by filtration through a nylon fiber column (NC) and E-rosette formation. Purified T and B cells contained less than 1% of other cell types. The responses of T cells to concanavalin A (Con A) and soluble protein A were greatly enhanced in the presence of autologous B cells. Participation of B cells in T-cell enhancement was confirmed by the following observations: (a) purified B copulation, which was separated further from adherent B cells, retained its enhancing activity. (b) Another adherent cell-free B-cell preparation, which was purified from the NC-passed fraction, and (c) no T lymphoid but some B lymphoid cell lines, elicited strong T-cell enhancement. It was also found that the enhancing capacity of B cells required no metabolic activity, but rather an intact cell form and direct cell-to-cell contact with responding cells. The stimulatory determinants on B cells were resistant to trypsin and neuraminidase treatment. In this paper a hypothesis will be presented that at least two signals are prerequisite for the effective activation of T cells.

B-Lymphocytes↗
PubMed1972

Cell interactions in the immune response in vitro. 3. Specific collaboration across a cell impermeable membrane.

Tissue cultures with two compartments, separated by a cell impermeable nuclepore membrane (1 micro pore size), were used to investigate the mechanism of T-B lymphocyte cooperation. It was found that collaboration was as effective when the T and B lymphocyte populations were separated by the membrane as when they were mixed together. Critical tests were performed to verify that the membranes used were in fact cell impermeable. The specificity of the augmentation of the B cell response by various T cell populations was investigated. Only the response of B cells reactive to determinants on the same molecule as recognized by the T cells was augmented markedly. Specific activation of thymocytes by antigen was necessary for efficient collaboration across the membrane. The response of both unprimed and hapten-primed spleen cells was augmented by the T cell "factor" although, as expected, hapten-primed cells yielded greater responses. The T cell factor acted as efficiently if T cells were present or absent in the lower chamber. Thus the site of action of the T cell factor was not on other T cells, but was either on macrophages or the B cells themselves. The T cell-specific immunizing factor did not pass through dialysis membranes. The experiments reported here help rule out some of the possible theories of T-B cell collaboration. Clearly T-B cell contact was not necessary for successful cooperation to occur in this system. Possible theoretical interpretations of the results and their bearing on the detailed mechanism of T-B lymphocyte cooperation are discussed.

Animals↗
PubMed1975

[The effect of hydrocortisone on individual stages of immunogenesis].

A study was made of the influence of hydrocortisone on the individual stages of immunogenesis: migration of the hemopoietic stem cells from the bone marrow, B-cell migration and cooperation between the T and B lymphocytes in the course of primary immune response to sheep red blood cells was studied. Experiments were carried out on (CBAXC57B1) F1 mice. In doses which failed to suppress the proliferation of hemopoietic cells hydrocortisone produced a marked immunosuppressive action which was a sum total result of its inhibition of various stages of immunogenesis--the stem cells and the B-cells migration and the T-B lymphocyte cooperation.

Animals↗
PubMed1980

In vivo cyclic change in B-lymphocyte susceptibility to T-cell control.

The humoral response to hapten-protein conjugates is an invaluable model for dissecting the cellular elements of lymphocyte cooperation, and the Mitchison secondary adoptive transfer system provides convincing evidence of cooperation between hapten-specific B cells and carrier-specific T cells in the production of anti-hapten antibody. Recently, attention has focused on the role of suppressor T cells in the regulation of antibody production. Several workers have shown that carrier-priming may, in some instances, suppress a subsequent hapten antibody response, both in vivo and in vitro. This effect is attributed to a suppressor T-cell population, generated during the initial phase of the immune response. Gershon and co-workers have postulated that such suppressor T cells function in a feedback regulatory loop to limit the duration of an immune response. We have examined the suppressive effect of carrier immunization in a secondary anti-hapten response in vivo and demonstrate a cyclic change in susceptibility of memory B cells to T-help and suppression. Such variation presents a severe restriction to any model of feedback control by suppressor T cells.

Animals↗
PubMed1979

Cooperation between subclass of T lymphocytes in the in vitro generation of cytotoxicity against a mutant H-2K difference. An analysis with anti-Lyt antisera.

The cellular requirements for the generation of cytotoxicity in mixed lymphocyte reaction (MLR) across an H-2K mutant difference were analyzed. Treatment of C57BL/6 lymphocytes with either anti-Lyt-1 or anti-Lyt-2 serum and complement strongly reduced their capacity to mount a cytotoxic response against the B6.C-H-2ba mutant. Almost complete reconstitution of the cytotoxic response occurred when a mixture of anti-Lyt-1 and anti-Lyt-2-treated cells was allowed to respond. Once cytotoxicity was generated, only anti-Lyt-2 serum affected it. It is concluded that in the cytotoxic response to the ba mutant, Lyt-1 helper cells collaborate with Lyt-2,3 killer cell precursors in the generation of Lyt-2,3 killer cells. Lyt-1,2,3 cells play, if any, a minor role in the generation of cytotoxicity. By comparison, the capacity to generate killer cells in MLR against an H-2K + IA difference was only affected by anti-Lyt-2 and not by anti-Lyt-1 serum, indicating that this response is relatively independent of help by Lyt-1 cells under the conditions tested.

Animals↗
PubMed1990

Natural history of stage A chronic lymphocytic leukaemia untreated patients. French Cooperative Group on Chronic Lymphocytic Leukaemia.

In chronic lymphocytic leukaemia (CLL), stage A was defined in 1979 as the best prognostic group of the three-stage (A, B, C) classification which was thereafter adopted by an International Workshop on CLL. Recently, the question of whether or not all stage A patients should be treated was raised by authors who described potential harmful effects of treatment among stage A patients and heterogeneity of stage A with respect to survival and disease progression. In this work, we studied the natural history of stage A-CLL in order to determine on which grounds a decision to treat should be made. We performed a prognostic study on 309 untreated stage A-CLL patients enrolled in a randomized clinical trial from 1980 to 1985. Our aim was to segregate a subgroup with a low probability of disease progression and death. We used three endpoints: overall survival (50 deaths), disease progression to stage B or C (78 events) and disease progression to stage C (39 events). Multivariate analyses, using Cox's model, selected nine variables as having a prognostic value for at least one endpoint, namely age, sex, general symptoms, involved axillary lymph node, splenomegaly, haemoglobin, platelets, lymphocyte count and bone-marrow infiltration. By considering the three endpoints jointly, we obtained a proposed definition of smouldering CLL based on four variables, namely haemoglobin level, lymphocyte count, the number of enlarged areas and bone-marrow infiltration. However, we did not succeed in better defining smouldering CLL than in a previous proposal, based on haemoglobin level and lymphocyte count. Moreover, whatever the definition used, including other previous works, disease progression within 5 years was still observed for about 10% of patients with smouldering CLL. Future attempts to define smouldering CLL could perhaps benefit from using biological markers.

Adult↗
PubMed2006

Costimulatory molecules and cytokine production by T lymphocytes in common variable immunodeficiency disease.

Common variable immunodeficiency (CVID) is a heterogeneous syndrome characterized by hypogammaglobulinaemia and recurrent infections. Although early works pointed to a primary B-lymphocyte defect as a cause of the disease, a failure in T-lymphocyte cooperation has also been suggested. T cells exert their costimulatory function through either membrane costimulatory molecules or secreted cytokines, both having an influence in the development of the humoral response. The aim of our study was to evaluate whether an abnormal expression and induction of costimulatory molecules or alterations in the production of cytokines by T cells cause deficient T/B cooperation in CVID patients. We studied the expression and upregulation of costimulatory molecules (CD28, CD40L/CD154 and CTLA-4/CD152) and production of cytokines (IL-2, IL-4, IL-6, IL-10, IFN-gamma and TNF-alpha) in purified T lymphocytes from CVID patients stimulated with optimal doses of anti-CD3 or suboptimal doses of anti-CD3 and anti-CD28. Stimulated T cells from CVID patients expressed normal levels of CD28, CD40L/CD154 and CTLA-4/CD152 when compared with controls. Except for higher production of IL-4 after stimulation with anti-CD3, T cells of CVID patients produced similar amounts of cytokines compared with controls. An imbalance between costimulatory molecules expression (CD28, CD40L/CD154 and CTLA-4/CD152) and cytokine production by T cells does not explain a deficient cooperation between T and B cells in this group of CVID patients.

Adult↗
PubMed1981

The differentiation of cytotoxic T cells in vitro. IV. Interleukin-2 production in primary mixed lymphocyte cultures involves cooperation between Qa-1+ and Qa-1- "helper" T cells.

Studies with C57BL/6-TIaa mice have established that both Qa-1+ and Qa-1- helper T cells are required for the optimal production of Interleukin 2(IL-2) activity in primary MLC. This was established both by depletion of Qa-1 bearing cells by treatment of responder cells with anti-Qa-1 serum in the presence of complement and by positive selection (using FACS II analysis) of those cells displaying Qa-1. Furthermore, microfluoremetry revealed that the great majority of C57BL/6-TIaa and of A/J splenic T cells bore Qa-1 alloantigen but that only those with the highest antigen density were susceptible to complement-mediated lysis.

Animals↗
PubMed1980

Essential and nonessential cooperative signals in lymphocyte triggering in solid cultures.

The kinetics of lymphocyte stimulation by mitogens in solid cultures were used to study the role of cell interactions in these responses. An absolute requirement for cell interactions, possibly through soluble mediators, was found in lymphocyte responses to calcium ionophore A23187, phytohemagglutinin HA17 and tetradecanoylphorbol acetate. Accessory leukocytes were adherent to plastic surfaces and did form E rosettes. Autologous erythrocytes were also capable of providing essential cooperative signals. 2-Mercaptoethanol, in contrast, only provided nonessential cooperative signals for lymphocyte stimulation in solid cultures.

Calcimycin↗