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PubMed1980

Mutual recognition of parental and F1 lymphocytes. Selective abrogation of cytotoxic potential of F1 lymphocytes by parental lymphocytes.

Four different combinations of F1 hybrid mice [(C57BL/10 X B10.A)F1, (C57BL/10 X B10.BR)F1, B6D2F1, and AKD2F1] were injected intravenously with spleen cells from parental strains. The T-cell-mediated cytotoxic potential of spleen cells from the injected F1 mice was assessed from 4 to 21 d later by in vitro sensitization with trinitrophenyl-modified parental or syngeneic F1 spleen cells (TNP-self) or with allogeneic spleen cells. The cytotoxic potential of the F1 mice to TNP-self as well as to alloantigens was abolished or severely depressed throughout this period when the respective H-2k,a,d parental spleen cells were injected. In contrast, the cytotoxic potential was unaffected or only marginally reduced when H-2b parental cells were injected. The induction of depressed cytotoxic activity was shown to be a result of a population of parental radiosensitive T lymphocytes. The results should be discussed with respect to (a) the genetic and mechanistic parameters associated with the differential depressive effects of parental cells expressing H-2b vs. H-2k,a,d antigens, and (b) the use of this system for investigating allogeneic receptors on T-lymphocyte populations.

Animals↗
PubMed1976

Generation of cytolytic T lymphocytes in vitro. VIII. failure of anti-RS antisera to inhibit the generation of cytolytic T lymphocytes or cytolytic T lymphocyte activity.

Antibody reactive with "recognition structures" (RS) of mouse lymphoid cells for alloantigens (anti-RS) was prepared by immunization of F1 hybrid mice with parentalstrain lymphoid cells or with antibody produced in one parental strain against alloantigens of the other parental strain. Such antisera prevented generation of the "product of antigenic recognition" (PAR) that is produced within a few hours in cultures prepared with a mixture of lymphoid cells from genetically disparate mice. However, treatment of responding lymphoid cells with anti-RS sera and complement did not inhibit generation of cytolytic T lymphocytes (CTL) in mixed lymphocyte cultures (MLC). Treatment of cells obtained from MLC with anti-RS sera and complement failed to inhibit cytolytic activity of such cells for specific alloantigens.

Animals↗
PubMed1978

Augmented mitotic response of human peripheral lymphocytes in the presence of lymphocytes from nude mice: detection of a small number of functional human lymphocytes in the explanted host.

In the present paper, authors showed a method to detect a small number of functional human peripheral lymphocytes (HPL) in the presence of lymphoid cells of nude mouse (n-ML). HPL was mixed with n-ML to give a total number of 5 X 10(4) cells and cultured in vitro in the presence of PHA for 5 days. HPL responded will to PHA while n-ML did not, as assessed by 3H-TdR incorporation in the presence of the mitogen. Synergistic response between these two cell population was observed. Five--ten folds enhancement was shown by mixing 5 X 10(3) HPL and 4.5 X 10(4) n-ML (10% of HPL) and 500 HPL became detectable by comixing with n-ML, while 5,000 HPL was the lowest limit to be detected in a single cell culture with this mitogen. The results seem to indicate that this method could detect functional HPL as small number as one percent of the cell mixture. On the other hand, xenogeneic mixed lymphocyte reaction was observed when the percentage of HPL exceeded 40%. Mitomycin-C treatment of either HPL or n-ML revealed that a major part of cells incorporating 3H-TdR was HPL which could be activated by the stimulation with xenogeneic murine nucleated cells and that a smaller part of murien B cells were also stimulated by the HPL.

Animals↗
PubMed1985

Lymphocytes from patients with hairy cell leukaemia enable the distinction of two separate subpopulations of activated lymphocyte killer cells generated in mixed lymphocyte culture.

Blood from patients with hairy cell leukaemia (HCL) was used to investigate subpopulations of the non-specific activated lymphocyte killer (ALK) cells generated in mixed lymphocyte culture (MLC). Mononuclear cells from four of five patients with HCL had decreased natural killer (NK) cell activity and, of these, all showed a decrease in ALK cell activity against K-562 target cells (NK like cells), but three had normal levels of ALK cells able to kill melanoma cells. One patient who had received splenectomy had normal NK cell activity, and in MLC his cells generated normal levels of both subpopulations of ALK cells. The results support the hypothesis of separate subsets of ALK cells: NK like cells with NK cell precursors and which preferentially lyse the K-562 target cell and a second separate population which arises independent of NK cell precursors and which has strong cytolytic activity against an NK insensitive melanoma cell line.

Cell Line↗
PubMed1997

Generation of primary tumor-specific cytotoxic T lymphocytes from autologous and human lymphocyte antigen class I-matched allogeneic peripheral blood lymphocytes by B7 gene-modified melanoma cells.

Expression of B7.1 costimulatory molecules on tumor cells has been shown to elicit antitumor immunity in mice. In the present study, we have developed a human B7.1 retroviral vector system to effectively transduce human melanoma cell lines and investigated the potential role of B7.1 in the generation of tumor-specific CTLs from peripheral blood lymphocytes (PBLs) in vitro. We have demonstrated that B7.1-modified melanoma cells are able to induce primary CTL activity from autologous, human lymphocyte antigen (HLA) class I-matched allogeneic PBLs and purified CD8+ T cells in the absence of exogenous cytokines. CTLs generated by B7.1 are tumor specific and HLA class I restricted, and CD8+ T cells are primarily responsible for this specific cytotoxicity. Furthermore, CTLs generated from HLA class I-matched PBLs by B7.1 are cytolytic to tumor cells autologous to the stimulated PBLs. These data suggest that B7.1-modified tumor cells can be used as a potent tumor vaccine for both autologous and HLA class I-matched allogeneic patients.

Animals↗
PubMed1989

MHC and non-MHC genes regulate elimination of lymphocytic choriomeningitis virus and antiviral cytotoxic T lymphocyte and delayed-type hypersensitivity mediating T lymphocyte activity in parallel.

The course of systemic infection with lymphocytic choriomeningitis virus was studied in mouse strains differing in the MHC or non-MHC background. Virus clearance rates differed significantly between H-2 identical strains as well as between congenic strains differing in the H-2L subregion, indicating that both H-2 and non-H-2 genes may influence the elimination of this virus. Differences in virus spread prior to appearance of the immune response could not explain the observed differences in clearance rate. On the other hand, inefficient clearance always correlated with low T cell responsiveness measured in terms of virus-specific cytotoxicity and delayed-type hypersensitivity, whereas no correlation was found with regard to NK cell activity and antiviral antibody response. Analysis of F1 progeny between H-2 identical high and low responder strains showed that low responsiveness with regard to all three parameters was recessive, indicating that natural tolerance is not the mechanism explaining non-MHC dependent low responsiveness in this system. The implications of these findings are discussed with specific reference to the role of MHC genes in controlling resistance to infectious diseases.

Animals↗
PubMed1977

K cell activity of normal and chronic lymphocytic leukaemia lymphocytes: association with lymphocytes bearing receptors for human C3b.

Blood lymphocytes of patients with chronic lymphocytic leukaemia (CLL) and of normal individuals were depleted of EAC3b- or EAC3d-rosette-forming cells (RFC), respectively and assayed for K-cell activity in a system measuring antibody-dependent-cell-mediated cytotoxicity (ADCC). K-cell activity was found to be associated with a cell population bearing receptors for C3b.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1989

Isolation and complete structure of the lymphocyte serine protease granzyme G, a novel member of the granzyme multigene family in murine cytolytic T lymphocytes. Evolutionary origin of lymphocyte proteases.

A cDNA clone that is closely related to the granule-associated serine proteases of cytolytic T lymphocytes (CTL), called granzymes A-F, was isolated from a CTL expression library. The encoded serine protease, granzyme G, shows 70%-89% nucleotide identities to the granzymes C-F and, like those, consists of 228 amino acids preceded by the short propeptide Glu-Glu and a 18 residue long signal peptide. Granzyme G was identified by amino-terminal sequence analysis as a correctly processed and sorted protein stored in lysosome-like granules. The phylogenetic history of the granzyme multigene family was reconstructed by two tree-making methods and by Southern blot analyses of human, rat, and mouse DNA. Our results indicate differences in the evolutionary pathway between these species. The murine granzymes C-G descended from a progenitor present at the time of mammalian radiation. Granzyme C branched off first after the primate-rodent split and was involved in a recombination event with granzyme B before the rat-mouse divergence. Granzymes D and E have diverged after the mouse-rat speciation. However, no experimental evidence for the existence of a granzyme C-D-E-F-G equivalent was found in humans, and loss of the ancestral gene in the primate lineage is discussed. In view of the species differences in the number of granzyme gene copies during recent evolution, we propose that the murine granzymes B-G play several distinct roles in CTL-mediated effector functions as a response to quite recent changes of the biochemical environment.

Amino Acid Sequence↗
PubMed1978

Studies on cell surface antigens of mouse leukemic and normal lymphocytes. IV. Functional studies on mouse T lymphocyte subpopulations. B. Lyt phenotype of cytotoxic T lymphocytes and their precursors in B6-Lyt-1.1 mice.

Lyt phenotype of in vitro generated alloreactive cytotoxic T lymphocytes (CTL) and their precursors in B6-Lyt-1.1 (Thy-1.2, Lyt-1.1, Lyt-2.2) congenic strain of mice was studied. The generation of CTL in vitro was completely abrogated by pretreatment of responder cells with antisera to Thy-1.2, Lyt-1.1 and Lyt-2.2 antigens and complement. Mixing of anti-Lyt-1.1-pretreated cells with anti-Lyt-2.2-pretreated cells did not restore CTL generation indicating that both Lyt antigens are expressed on the same precursor cell population. The effect of anti-Lyt sera was specific because the generation of CTL was prevented only when cells from strains possessing appropriate Lyt alleles were pretreated. CTL were eliminated by lysis with anti-Thy-1.2 serum and strongly reduced by anti-Lyt-1.1 and anti-Lyt. 2.2 sera. Nevertheless, a small but significant proportion of CTL was insensitive to lysis with anti-Lyt sera. These data indicate that a phenotype of precursor cells and of majority of CTL is Thy-1.2+ Lyt-1.1+ Lyt-2.2+.

Animals↗
PubMed1980

Subpopulations of human T lymphocytes. XV. T lymphocytes with receptors for IgA (T alpha), a distinct subpopulation of T lymphocytes. Studies in patients with primary immunodeficiency disorders.

A receptor for IgA was observed on a subset of T cells (T alpha) that is distinct from other T lymphocyte subsets, T mu or T gamma cells. IgA receptor on T alpha cells is blocked by IgA from human serum through its cytophilic attachment. Neither T mu nor T gamma cells, following an in vitro interaction with insoluble immune complexes during the process of purification and further incubation at 37 degrees C, changed their phenotypes to T alpha cells. However, some T gamma cells demonstrated transition to T mu cells. The numbers and proportion of T alpha cells in patients with selective IgA deficiency were either normal, increased or decreased. The significance of T alpha cell analysis in thirty-one patients with primary immunodeficiency disorders including those with selective IgA deficiency is discussed.

Antigen-Antibody Complex↗
PubMed1980

Phagocytosis and lymphocyte migration: evidence that lymphocyte trapping in the spleen following carbon injection is not due to direct lymphocyte-macrophage adherence.

The localization of intravenously injected labelled syngeneic lymphoid cells was studied in the spleen of mice and compared with the localization of Indian-ink-containing macrophages. To distinguish between Indian-ink-containing lysosomes of macrophages and silver grains formed in the autoradiographs over the radiolabelled cells, the latter grains were stained blue by a colour-coupling process. Labelled cells were injected 2 h after the Indian ink. Two hours after their injection the bulk of the labelled cells in the spleen was already localized in the white pulp. At this time the Indian ink had been ingested by macrophages in the marginal zone and to a somewhat lesser extent in the red pulp. Twenty-four hours after injection of the cells their concentration in the white pulp appeared constant or had decreased markedly, dependent on the source of the injected cells (spleen, lymph nodes or thymus). At this time carbon-containing macrophages were also found in the white pulp although they contained less carbon than macrophages in the marginal zone and red pulp. A positive correlation between labelled cells and carbon-containing macrophages was never seen in any part of the spleen. It is concluded that, if carbon-containing macrophages induce lymphocyte trapping, as has been supposed by other authors, this trapping must be mediated by the macrophages in an indirect way, e.g. by soluble mediator molecules released in the circulation.

Animals↗
PubMed2001

Mechanisms of mouse T lymphocyte-induced suppression of the IgG2ab allotype and T lymphocyte tolerance to IgG2ab.

In mice of the Igha immunoglobulin allotypic haplotype we found, the presence of T lymphocytes with an inherent inhibitory activity against the expression of the IgG2a(b) allotype (IgG2a of the Ighb immunoglobulin allotypic haplotype). This constitutive anti-IgG2a(b) T lymphocyte activity can be enhanced in vivo by what we called "sensitization", which usually consists of one or two intravenous injections of B splenocytes from Ighb congenic mice. When injected at birth, the resulting anti-IgG2a(b) T splenocytes induce, with 100% success, total, specific and chronic (but experimentally reversible) suppression of IgG2a(b) in Igh(a/b) F1 hybrid mice prepared by mating Igh congenic mice. Even if restricted to IgG2a(b) expression, this experimental model, which deals with an unambiguous case of T cell-mediated down-regulation of immunoglobulin production, provides a clear and powerful tool to dissect finely the behavior of the partners (T and B lymphocytes) intervening in regulation within the immune system. For example, we observed that CD4 T lymphocytes were necessary to obtain full recruitment of anti-IgG2a(b) CD8 T lymphocytes during the sensitization, that suppression induction in anti-IgG2a(b) T splenocytes of newborn recipients required cooperation between CD4 and CD8 T lymphocytes, and that CD8 T lymphocytes were essential for suppression maintenance. We showed that this suppression was not characterized by an accumulation of B lymphocytes containing the allotype they could not secrete or Cgamma2a(b) mRNA they could not translate. The recipient's immune system was not involved in the suppession maintenance; this was done by donor T lymphocytes, which ensured the chronicity of IgG2a(b) suppression throughout the recipient's life. We demonstrated that the mechanism of this suppression implied an MHC-restricted presentation by target B lymphocytes of Cy2a(b) peptides to the T cell receptor (TCR) of anti-IgG2a(b) T lymphocytes. Notwithstanding the requirement of a CD4-CD8 T lymphocyte cooperation during the induction phase, we functionally determined that the suppression induction implicated an MHC class I-, but not class II-restricted interaction. We also demonstrated the existence in vivo of alternative or concomitant use of perforine- and Fas-mediated cytotoxicity pathways in this T cell-induced IgG2a(b) suppression. Thus this suppression did not imply silencing IgG2a(b) production, but B lymphocyte destruction by CD8 T lymphocytes. Always using our suppression model, we demonstrated that an agonistic anti-CD40 treatment helps in recruiting CD8 cytotoxic T lymphocytes, involved in immune regulatory functions and that CD40 expression on Ighb B lymphocytes confronted with CD8 T lymphocyte effectors only operating via the Fas pathway was involved in the total suppression of IgG2a(b) expression. The selection and maintenance of such normal T cell activity against the IgG2a(b) allotype in mice of different genetic backgrounds remain somewhat enigmatic. Indeed, we did not observe any similar activity against other immunoglobulin allotypes or isotypes. The intestinal flora had no influence on the emergence of this anti-IgG2a(b) T lymphocyte activity, as it was untouched in germ-free-Igha mice when compared with normal Igha mice. More recently, this model offered an opportunity to study problems pertaining to immune tolerance. For instance, we showed that the genetic elements involved in the building of anti-IgG2a(b) TCR were available in Igha and Ighb mice of different genetic backgrounds, but that somatic constraints, namely the perinatal presence of IgG2a(b), effectively prevented their acquisition, while its absence led to their spontaneous emergence. Consequently, we were able to induce anti-IgG2a(b) T lymphocytes into a tolerance state by injecting Igha mice with soluble IgG2a(b) during the perinatal period. However, the full T lymphocyte tolerance obtained in this manner was not definitively acquired, as it had reversed spontaneously when investigated 3 to 6 months after the end of tolerogen treatment, even when this treatment had been prolonged from the perinatal period to 9 months of age. The mechanisms (induction and reversion) of this tolerance involves the physical elimination or the irreversible inactivation of the natural anti-IgG2a(b) T lymphocyte clones and their resurgence, from bone-marrow precursors, as long as the thymus remains operational, but not the establishment of a reversible, functional unresponsiveness (anergy) or an active, cell-mediated inhibition of anti-IgG2a(b) T clones. We attempted to elucidate, in Ighb mice, whether the natural T lymphocyte unresponsiveness to IgG2a(b) involved a central tolerance mechanism and to identify the type of tolerogen implicated in this tolerogenesis. The experiments principally showed that this natural T lymphocyte tolerance to IgG2a(b) was mediated by a thymic mechanism; that the capacity to induce it was gradually acquired by Ighb thymuses and was most probably due to potentially IgG2a(b)-producing/presenting cells, progressively colonizing the developing thymus; and that a significantly decreased postnatal Cy2a(b) gene transcription correlated with the emergence of anti-IgG2a(b) T lymphocytes in Igh(a/b) F1 (postnatally deprived of their B lymphocyte compartment), which subjected them to autoimmune IgG2a(b)-allotype suppression.

Animals↗
PubMed1988

Human epidermal cells from ultraviolet light-exposed skin preferentially activate autoreactive CD4+2H4+ suppressor-inducer lymphocytes and CD8+ suppressor/cytotoxic lymphocytes.

In vivo exposure of human epidermis to UV abrogates the function of T6+DR+ Langerhans cells and induces the appearance of Ag-presenting T6-DR+ OKM5+ cells in the epidermis. Since UV exposure of murine skin results in Ts lymphocyte activation, we investigated the capacity of human epidermal cells (EC) harvested 3 days after in vivo UV exposure to activate regulatory and effector autologous T lymphocyte subsets. T lymphocytes were separated into CD8+ suppressor/cytotoxic lymphocytes and CD4+ helper/inducer lymphocytes by C lysis and panning. The CD4+ subset was further divided by using the 2H4 mAB to obtain CD4+2H4+ lymphocytes (inducers of TS lymphocytes) and CD4+2H4- lymphocytes (inducers of B cell Ig production and inducers of cytotoxic T cells). Unirradiated suction blister-derived EC from control skin (C-EC) and from skin exposed in vivo to UV (UV-EC) were cultured with purified autologous T lymphocyte subsets in the absence of added Ag. The resultant T lymphocyte proliferation was detected by [3H]thymidine uptake. UV-EC were highly effective in the stimulation of CD4+ lymphocytes, whereas C-EC were poor stimulators. The stimulator effect of UV-EC was abrogated after depletion of DR+ UV-EC. When CD4+ lymphocytes were fractionated, UV-EC consistently demonstrated enhanced ability to stimulate suppressor-inducer CD4+2H4+ lymphocytes relative to C-EC. Although less responsive than CD4+2H4+ lymphocytes, CD4+2H4- lymphocytes also demonstrated greater proliferation to UV-EC than to C-EC. Neither UV-EC nor C-EC were able to activate CD8+ lymphocytes devoid of CD4+ lymphocytes. However, after addition of rIL-2 at concentrations that allow binding only to the high affinity IL-2R on T lymphocytes, UV-EC induced vigorous proliferation of CD8+ lymphocytes, whereas C-EC induced only background levels of proliferation. C lysis of leukocytes resident within UV-EC resulted in 66 to 70% reduction of CD8+ lymphocyte proliferation. In conclusion, UV-EC may activate CD8+ lymphocytes by at least two pathways: (1) UV-EC activation of CD4+2H4+ lymphocytes may induce differentiation/proliferation of CD8+ suppressor cells and (2) UV-EC activation of CD4+ cells may induce IL-2 production, that, in combination with UV-induced epidermal leukocytes, stimulates CD8+ cells.

Adult↗
PubMed1994

Phenotypic characterization of human B-lymphocyte subpopulations, particularly human CD5+ B-lymphocyte subpopulation within the mantle zones of secondary follicles.

We have investigated the precise distribution of human B-lymphocyte subpopulations (CD5+ B lymphocyte, Leu-8+ lymphocyte, immunoglobulin D (IgD)+ lymphocyte, alkaline phosphatase (ALPase)+ B lymphocyte and bcl-2 protein+ B lymphocyte) within the mantle zones (MZs) and phenotypic characterization of human CD5+ B lymphocytes using immunohistochemical techniques and flow cytometric analysis. IgD+ lymphocytes and ALPase B lymphocytes were confined to the inner layer and outer layer of the MZs of secondary follicles, respectively. CD5+ B lymphocytes and Leu-8+ B lymphocytes were mostly located in the inner layer of the MZs. Bcl-2 protein+ B lymphocytes were seen throughout the MZs. The precise distribution pattern of human B-lymphocyte subpopulations may help further understanding of the histogenesis and features of B-cell lymphomas, particularly mantle cell-derived lymphomas as well as the B-cell differentiation pathway. A minor population of CD5+ B lymphocytes expressed IgD. Almost all the CD5+ lymphocytes did not express ALPase. The data support the fact that CD5+ B lymphocytes are located more in the inner layer than in the outer layer of the MZs. Leu-8 and bcl-2 protein were detected in a large population of CD5+ B lymphocytes. In addition, Ki-67 antigen was not expressed on the CD5+ B lymphocytes. The data suggest that human CD5+ B lymphocytes may be long-living and resting (G0 and G1a stage) cells possessing the capability of continuously recirculating between blood and lymph nodes to participate in some immune responses. Moreover, Leu-8 and CD44 were detected in the majority of CD5+ B lymphocytes but intercellular adhesion molecule-1 (ICAM-1) and very late antigen-4 (VLA-4) were detected in the minority. The data may account for a high percentage of Leu-8 and CD44 expression and a low percentage of ICAM-1 and VLA-4 expression on B-chronic lymphocytic leukemia (B-CLL), which is considered to be a neoplastic counterpart of normal CD5+ B lymphocyte.

Antigens, CD↗
PubMed1979

Adenylate cyclase in thymus-derived and bone marrow-derived lymphocytes from normal donors and patients with chronic lymphocytic leukemia.

Lymphocytes were purified from peripheral blood of normal donors and patients with chronic lymphocytic leukemia (CLL) by Ficoll-Hypaque centrifugation. Adenylate cyclase activity, expressed as picomoles [(32)P]cyclic AMP generated per milligram protein per minute, was 57+/-4 in normals and 26+/-4 in CLL patients. Enzyme activity, expressed as picomoles [(32)P]cyclic AMP generated per 10(6) lymphocytes per minute, was 2.09+/-0.19 for normal lymphocytes and 1.10+/-0.16 for CLL lymphocytes. The differences between normal and CLL peripheral lymphocytes are highly significant (P < 0.001) with either method of calculating activity. Cyclic AMP levels (picomoles per 10(6) lymphocytes) also differed significantly: 1.38+/-0.29 for normals and 0.45+/-0.08 for CLL lymphocytes. Adenylate cyclase was assayed in lymphocytes enriched for bone marrow-derived (B) cells by removing E-rosetted thymus-derived (T) cells, and enriched for T cells by harvesting E-rosetted lymphocytes or by removing B cells with nylon wool absorption. Solutions to simultaneous equations gave the following calculated enzyme activities for pure B- and T-cell subpopulations (in picomoles [(32)P]cyclic AMP generated per milligram mg protein per minute): normal B, 196+/-22; normal T, 30+/-10; CLL B, 34+/-6; CLL T, 19+/-4. Thus. normal B-lymphocyte adenylate cyclase exceeds normal T-lymphocyte activity by more than sixfold, whereas in the case of CLL the enzyme activity in B lymphocytes is markedly reduced to levels comparable to T lymphocytes. The responses of lymphocytes to stimulation with the hormones prostaglandin E(1) and isoproterenol, and with NaF, were assessed. Compared with normal lymphocytes, enzyme activities were reduced in CLL lymphocytes incubated with these agents, but to a degree paralleling the reduced basal activities. Thus, the ratios between stimulated and basal adenylate cyclase levels in Ficoll-Hypaque-purified, normal lymphocytes were 2.3+/-0.1 after incubation with 10 muM isoproterenol, and 3.9+/-0.2 with 10 mM NaF, values which did not differ significantly from those obtained with CLL lymphocytes. When the enzyme activities calculated for purified T- and B-lymphocyte subpopulations were used to derive the stimulation ratios, the responses of normal and CLL T and B cells to these agents were also indistinguishable. The simplest explanation for these findings is a reduced number of normally responsive enzyme sites on the surface membranes of CLL lymphocytes, although alternative explanations are possible.

Adenylyl Cyclases↗