Production of migration inhibition factor (MIF) and an inducer of plasminogen activator (IPA) by subsets of T cells in MLC.
Explore the source record for details and available documents.
Animals↗
SEARCH · PubMed Health
Results for “T-Lymphocyte Subsets”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Two functionally distinct subpopulations of human T cells that collaborate in the generation of cytotoxic cells responsible for cell-mediated lympholysis.
A human thymus-dependent differentiation antigen, TH2 was defined by a rabbit anti-human T cell serum absorbed with autologous B lymphoblasts and leukemic cells bearing T cell markers from a patient with chronic lymphocytic leukemia. Anti-TH2 reacted specifically with thymus-derived lymphoid cells and exhibited two distinct profiles of reactivity with normal peripheral T cells as detected by indirect immunofluorescence on a FACS I. Isolation of strongly reactive, TH2+, from weakly reactive, TH2- T cells by fluorescence-activated cell sorting revealed that the TH2+ subset contained most of the killer activity in cell-mediated lympholysis (CML), but had a diminished response in MLC and a suboptimal or negligible proliferative response to soluble antigens (mumps, PPD, tetanus toxoid). In contrast, the TH2- subset contained markedly less killer activity but amplified cytotoxicity by TH2+ cells and exhibited a proliferative response to both alloantigen and soluble antigens that was often significantly greater than the response by unseparated T cells. The relevance of these findings to previously described human T cell subsets and to functional subpopulations of murine T cells is discussed.
Absorption↗
Functional depletion of T- and B-memory cells and other lymphoid cell subpopulations-during trypanosomiasis.
T. brucei infection in mice causes generalized immunosuppression with multiple changes in the cells of the lymphoid tissue. Loss of B cell responsiveness to antigens and mitogens, and the induction of suppressive T-cells and macrophages, have been previously reported (Hudson, Byner, Freeman & Terry, 1976; Corsini, Clayton, Askonas & Ogilvie, 1977; Jayawardena & Waksman, 1977). In this study, purified B- or T-cell populations from infected mice have been tested functionally in vitro or in vivo by transfer into syngeneic irradiated hosts to separate the cells from trypanosomes or their products. B-memory cells for thymus dependent (DNP-KLH) and thymus independent (DNP-Ficoll) antigens are depleted or lose their potential to respond to the antigen during T. brucei infection. Similarly, purified T-helper cells, and T-cells reactive to allogeneic target cells in mixed lymphocyte reactions are functionally defective. By 16 days of infection all these responses are less than 10% of the normal level. The loss of B-cell function follows the peak parasitaemia and is accompanied by increases in the serum levels of both IgM and IgG. Enhanced Ig production and decline in B-cell potential also occur in T-deprived mice and in CBA/N mice which lack a subset of T-independent B-cells. Cells affecting delayed hypersensitivity reactions retain their activity throughout trypanosome infection and so far provide the only exception to the general decline in immune potential.
Animals↗
Con A-inducible suppression of MLC: evidence for mediation by the TH2 + T cell subset in man.
Human peripheral lymphoid cells pretreated with Concanavalin A for 48 hr can markedly suppress the proliferative response of untreated autologous lymphoid cells in MLC. Isolation studies with Sephadex G-200 anti-F(ab')2 affinity chromatography, nylon adherence, and E rosetting indicate that the Con A-induced suppressor cell is a T cell. Further fractionation into TH2+ and TH2- cell subsets with an equine-anti TH2 serum show that both subsets can be activated by Con A to an equivalent degree. After activation only the TH2+ subset can suppress autologous responder cells in MLC. The TH2- subset, which comprises 80% of peripheral human T cells, although induced by Con A to proliferate, cannot itself suppress the MLC response. Nevertheless, the TH2- subset can be shown to modulate the generation of suppressor TH2+ cells at 24 hr but not at 48 hr. These studies support the notion that the Con A-induced suppressor cell is confined to a distinct T cell subset in man and that T-T interactions are important in the overall expression of the immune response.
Adult↗
DRw antisera react with activated T cells.
Nylon wool-purified T cells appear to be nonreactive in a lymphocytotoxicity assay with HLA-DRw antisera and complement before cell activation. However, after activation in mixed lymphocyte culture, responder cells express determinants that are strongly reactive with DRw alloantisera after 6 days and gradually disappear by 16 to 18 days. Restimulation of the primed cells resulted in re-expression of the blast determinants. Mitogenic stimulation with Con A or purified PHA (HA-17) also resulted in temporary expression of these determinants; reactivity usually conformed to DRw genetic restriction; however, occasional extra reactions occurred that were variable depending on the method of activation (i.e., MLC, Con A, or HA-17). The results suggest the presence of additional allospecificities within some of the DRw antisera that react with "Ia-like" antigens on activated cells from unique subsets of T cells. Whether these DRw antisera contain antibodies against T cells or agains activation or differentiation T cell antigens is not as yet clear.
Adult↗
Surface properties and in vitro functional capacities of human T lymphocyte subsets separated by linear density gradients.
Human lymphocytes derived from various central and peripheral sources were separated on linear density gradients (LDG). Cells from individual density fractions were tested in parallel for: the capacity to form nonimmune rosettes with neuraminidase-treated SRBC, the number of surface-associated HTLA, and in vitro proliferative responses to mitogenic lectins and alloantigens. Heterogeneous density distribution profiles were obtained for all sources of human T cells and revealed an organ specificity. The various T cell density classes obtained from identical organs as well as the identical density classes of different sources revealed to some extent differences in their surface marker patterns and/or their in vitro reactivities. On the basis of the combined techniques at least two major subsets among thymocytes were identified that differed in both surface properties and functional capacities. Density classes of T cells from all peripheral sources were distinguished from thymocytes by a homogeneous lowered HTLA expression. Whereas clear-cut differences in the in vitro functional capacity were observed between the two thymocyte subsets, less striking but still significant differences were found to exist among the various density classes of peripheral T cells.
Animals↗
Active suppression of B lymphocyte maturation by two different newborn T lymphocyte subsets.
Explore the source record for details and available documents.
Adult↗
Ultrastructural, cytochemical, and membrane surface marker characteristics of the atypical lymphocytes in infectious mononucleosis.
Atypical lymphocytes from nine young adults with acute infectious mononucleosis (IM) were studied for morphologic, ultrastructural, cytochemical, and membrane surface marker characteristics. There was an absolute increase in T lymphocytes in the patients. Atypical lymphocytes accounted for 83%-96% of the lymphocyte population. These lymphocytes contained cytoplasmic inclusions which ranged in size from 1000 to 6000 A, were usually membrane bound, and consisted of parallel arrays of microtubulelike structures. The inclusions, which have been referred to as parallel tubular arrays (PTA), were found in 15%-75% of the lymphocytes from the IM patients. Ultrastructural cytochemical methods demonstrated acid phosphatase activity within many of the membrane-bound PTA. The function of the PTA is unknown. Since they were observed only in the lymphocytes which appeared to correspond to the atypical lymphocytes on light microscopy, the majority of which typed as T cells, there appears to be an association between PTA and T lymphocytes. It is possible that PTA identify a specific subset of T lymphocytes which is expanded in IM. Alternatively, PTA may be a transient finding in lymphocytes appearing only in certain biologic states of the cell such as during T-lymphocyte activation.
Acid Phosphatase↗
Functional differentiation of B lymphocytes in agammaglobulinemia. III. Characterization of spontaneous suppressor cell activity.
The addition of fresh peripheral blood mononuclear cells (PBL) from four of seven patients with agammaglobulinemia to generated hemolytic plaque-forming cells (PFC) resulted in a dose-dependent suppression of PFC. This spontaneous suppressor cell activity (SSA) was restricted to the four patients who could generate a PFC response in vitro. SSA was mediated by a small subset of E-rosetting T lymphocytes characterized by theophylline-sensitive E-receptors and surface receptors for Fc-IgG. The effects of SSA were temperature dependent and reversible, and pokeweed mitogen could prevent the rapid decline of SSA observed during culture. Augmentation of SSA was achieved by agents known to increase intracellular levels of cyclic AMP, whereas lithium chloride abrogated SSA, including the drug-induced effects. Cells mediating SSA may play a role in preventing the normal transition of pre-B cells to B cells in patients with agammaglobulinemia without B lymphocytes.
Agammaglobulinemia↗
Local xenogeneic graft-vs-host reaction: a practical assessment of T cell function among cancer patients.
The local xenogeneic graft-vs-host reaction (XGVHR) was used as a practical bioassay to assess T lymphocyte function and immunocompetence among cancer patients. Positive XGVHR was found in 99.5% of normal donors, 70% of cancer patients with early stage disease, and 30% of cancer patients with metastatic disease (p less than 0.001). A minimum of 4.5 x 10(6) immunocompetent T lymphocytes are necessary in order to elicit a positive XGVHR. Negative reactions among cancer patients are characterized by the lack of edema fluid accumulation and the appearance of the most basophils at the test site. This suggests that insufficient amounts of lymphokines are being released by the incompetent T lymphocytes, whereas the host is capable of mounting a rejection reaction as evidenced by the appearance of the basophils. Preliminary evidence suggests that the immunologic defect detected by the XGVHR cannot be corrected by monocyte depletion. The identification of putative suppressor T cell subsets may bear immunotherapeutic implications in the future.
Animals↗
Casein-induced experimental amyloidosis. V. The response of lymphoid organs to T and B mitogens.
Functional and morphologic studies were performed on the lymphoid organs of inbred CBA/J mice receiving chronic casein administration. In the spleen, this regimen produces marked reticuloendothelial proliferation between 8 and 16 injections (preamyloid phase) and amyloid deposition between 16 and 24 injections. No amyloid was found in the thymus, lymph nodes, and bone marrow of these animals. Phytohemagglutinin and concanavalin A lymphocyte responses as measured by 3-H-thymidine incorporation were reduced in the spleen and lymph node of preamyloid animals but demonstrated partial recovery during the amyloid phase. Phytohemagglutinin and concanavalin A stimulation of thymic cells was significantly increased during both stages of amyloid induction, although the histologic studies revealed a marked involution of the thymic cortex. Lipopolysaccharide stimulation of spleen cells was normal in preamyloid and amyloid animals whereas in lymph node and bone marrow lipopolysaccharide responses were significantly decreased. The findings suggest a selective removal of subsets of T cell populations in the spleen and thymus and migration of B cells from bone marrow to the spleen during experimental amyloidosis.
Amyloidosis↗
Immunological activities of rat lymphocytes. I. Mitogenic responses and surface markers of lymphocytes from normal, thymectomized and B rats.
Lymphocytes from the peripheral blood, thoracic duct, spleen and lymph nodes of normal, thymectomized (TX) and thymectomized lethally irradiated marrow reconstituted (TXBM or B rats) Lewis rats were studied for their ability to proliferate in vitro in the presence of Con A or PHA. At the same time the lymphoid tissues of these animals were examined for the presence of B cells or T cells by immunofluorescence staining with antiserums to rat immunoglobulins or rat brain antigens (ARBS), respectively. The specificity of ARBS fort T cells was first established in both cytotoxicity and immunofluoresecnce studies with thymocytes as well as pruified T and B cells. In various lymphoid tissues from TX and B rats, cells carrying brain antigens were found which were unable to respond to Con A and PHA. Thymectomy has a lesser effect on the response to Con A that to PHA; this was particularly true in the thoracic duct where, following thymectomy, lymphocytes continued to respond to Con A but lost their ability to respond to PHA. This suggests that the response to PHA and Con A may belong to different cells' subsets but that the ability to respond to either one of these mitogens may be impaired in cells carrying known T cell markers.
Animals↗
Ala-1: murine alloantigen of activated lymphocytes. II. T and B effector cells express ala-1.
Ala-1 (activated lymphocyte antigen-1) is a murine alloantigen expressed only on activated peripheral T and B lymphocytes. The presence or absence of Ala-1 on specific functional lymphocyte subsets was determined by treating the relevant cell population with anti-Ala-1 and complement, and assaying for residual functional activity. By this method, Ala-1 was shown to be on in vivo primed killer T cells cytotoxic for allogeneic tumor cells. It was also found on helper T cells generated in vivo to sheep red blood cells, and on IgM and IgG plaque-forming cells (PFC) to sheep red blood cells. In contrast, splenic precursors of helper cells and of IgM PFC to sheep red blood cells were completely resistant to treatment with anti-Ala-1 and complement. These findings indicate that effector cells can be distinguished from their nonactivated precursors by their expression of Ala-1.
Animals↗
Adherent cell function in murine T lymphocyte antigen recognition. II. Definition of genetically restricted and nonrestricted macrophage functions in T cell proliferation.
The mechanisms by which adherent cells, presumably of mononuclear phagocytic lineage, influence in vitro antigen-specific activation of murine T lymphocytes was examined. Two distinct functions for macrophages could be discerned. One macrophage function is dependent on a soluble factor produced by cultured adherent cells and is most easily studied with complex multideterminant antigens. This factor is neither antigen-specific nor MHC-restricted in its action in that PEC, regardless of haplotype, produce factor in the absence of antigen. A second function, antigen-specific T cell activation, is seen when antigens of more restricted heterogeneity are used, such as those under the control of Ir genes. This latter activity demands identity or partial identity between the antigen-presenting cell and the primed T cell, thus suggesting an additional specific, genetically restricted function for macrophages in in vitro antigen recognition. Whether these adherent cell functions are mediated by all or distinct subsets of cells was not established.
Animals↗
Human tumor-lymphocyte interaction in vitro. VI. Specificity of primary and secondary autologous lymphocyte-mediated cytotoxicity.
A T-cell-enriched lymphocyte subset of samples from 15 tumor patients was tested for primary cytotoxicity against autologous tumor cell preparations and against 1-3 different allogeneic tumor cell preparations from biopsy material. Allogeneic cytotoxicity occurred in only 1 of 10 patients with autologous reactivity. The lymphocytes of 14 patients were cultured with autologous cells from biopsy material for 6 days. These lymphocytes killed autologous targets, but only 1 patient's lymphocytes were cytotoxic against 1 of the 4 allogeneic tumors tested. Cocultivation with allogeneic cells from biopsy specimens generated cytotoxicity toward the sensitizing allogeneic cells in 3 of 9 test combinations. In 2 of 3 instances the effectors were also active against the autologous tumor cells. Cytotoxicity in primary and secondary tests occurred thus only rarely against allogeneic targets. This indicated either the presence of individual tumor-related antigens on the cells from biopsy material or reflected the histocompatibility restriction of T-cell-mediated cytotoxicity.
Antigens, Neoplasm↗
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↗
B-cell subsets responsive to fluorescein-conjugated antigens. III. Differential effect of E. Coli lipopolysaccharide on T-dependent and T-independent responses in vivo.
The effect of E. coli lipopolysaccharide (LPS) on the induction of both hapten-specific immunity and tolerance was studied in an in vivo system utilizing putative T-cell dependent (TD) or T-cell independent (TI) challenge antigens. The administration of LPS 1 day prior to challenge preempted the response of C3D2 mice to a TD antigen (FL-KLH) but had little effect on the response to FL-Ficoll, a TI antigen. LPS did not affect the responsiveness of C3H/HeJ mice, an LPS-unresponsive strain, to either antigen. The reduction of the response to a putative T-dependent antigen by LPS pre-treatment was only temporary since mice challenged 7 days after LPS responded normally in vivo. We also confirmed that LPS administered shortly after a tolerogen prevented FL-specific IgG tolerence induction and produced B-cell priming to a subsequent T-dependent antigenic challenge. LPS, however, did not significantly interfere with tolerance induction in terms of the IgM responce to either challenge antigen. These results suggest that LPS acts either directly or indirectly on a subpopulation of B cells responsive to a TD antigen. Our data further reflect the heterogeneity of B-cell subpopulations responsive to various polyclonal activators.
Animals↗
Preferential induction of memory T cells for delayed-type hypersensitivity with reduced and alkylated human serum albumin in mice.
Reduction and alkylation of human serum albumin (HSA) resulted in molecular aggregation of the protein. The reduced and alkylated antigen (RA-HSA) was lacking in the ability to induce delayed-type hypersensitivity (DTH) response as well as antibody response to native HSA in mice, although native HSA induced both responses. On the other hand, RA-HSA could stimulate a priming function that accelerated and enhanced the DTH response to native HSA, which, however, failed to stimulate the function. Thus, DTH-related memory activity was dissociated from DTH-related effector activity. The DTH-related memory activity, manifested by the accelerated an enhanced response in RA-HSA-primed mice, could be transferred antigen-specifically by their spleen cells and T-cell enriched fraction, but not by their T-cell depleted spleen cells. The RA-HSA-primed T cells, however, failed to transfer the effector function for DTH response. These results suggested that DTH-related memory T cells belong to different subset(s) of T cells from effector T cells for a DTH response.
Animals↗