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At least 19 recordsLinked to original sources
PubMed1976

Antibodies to guinea pig lymphokines. II. Suppression of delayed hypersensitivity reactions by a "second generation" goat antibody against guinea pig lymphokines.

A "second generation" antibody to a highly purified lymphocyte product was raised in a goat against material eluted from a rabbit anti-guinea pig lymphokine immunoadsorbent column. This anti-lymphokine serum, in constrast to anti-lymphocyte serum (ALS) did not appear to contain cytotoxic antibodies directed against membrane antigens on guinea pig lymph node lymphocytes. Furthermore, the anti-lymphokine serum did not inhibit the formation of spontaneous T rosettes nor significantly depress lymphocyte response to mitogens. The anti-lymphokine serum totally suppressed the delayed skin reactivity to PPD and contact sensitivity to DNCB when injected intradermally around the site of antigen challenge. By contrast, intradermally injected ALS did not appear to suppress the PPD response in sensitized guinea pigs. Intravenously and i.p. administered anti-lymphokine serum was somewhat less effective in suppressing the delayed skin response to PPD. The intradermal injection of the antiserum had no effect on nonspecific inflammation evoked by turpentine-olive oil or on the extravasation of circulating Evans blue evoked by intradermally injected histamine. Histologic examination of 24-hr DNCB-induced skin lesions from sensitized guinea pigs treated with intradermally injected anti-lymphokine serum showed marked reduction of mononuclear infiltration of the dermis and of epidermal lesions, as compared with skin sites taken from sensitized animals pretreated with normal goat serum. The anti-lymphokine serum injected i.v. also markedly reduced the perivascular infiltration of the dermis and subcutis in skin reaction sites from sensitized animals challenged with PPD. Intravenous treatment with ALS for 3 consecutive days caused extensive depletion of the paracortical areas of peripheral lymph nodes whereas treatment with normal serum and anti-lymphokine serum caused no such depletion. It is proposed that the anti-lymphokine serum is directed against activated lymphocyte products, one of them being MIF. These products are involved in the mediation of delayed hypersensitivity reactions. This is in marked contrast to ALS, the suppressive action of which appears to be central rather than peripheral.

Animals↗
PubMed1992

Enhanced lymphokine production and lymphokine receptor expression in multiple antibody-stimulated human CD4+ peripheral blood lymphocytes.

Treatment of T lymphocytes with antibodies directed against the T cell receptor CD3 complex results in cellular activation that can be augmented by costimulation through other cell surface receptors. The activities of anti-CD3-stimulated human CD4+ PBL were compared to anti-CD3 plus anti-CD2-, anti-CD4-, or anti-CD11a (LFA-1)-stimulated cells. [3H]thymidine incorporation, lymphokine receptor expression, expansion of cell numbers, and lymphokine mRNA and protein were measured. Forty-eight hours after activation, costimulated CD4+ cells demonstrated increased numbers of cells positive for surface IL-2R alpha-chain, IL-2R beta-chain, IFN-gamma receptors, and TNF-alpha receptors. By day 6, costimulated cells exhibited a sevenfold greater expansion in cell numbers compared to cells stimulated with anti-CD3 alone. Anti-CD3 plus anti-CD11a stimulation consistently induced the highest secretion of IL-2 and IFN-gamma, whereas variation in secretion of TNF-alpha and IL-4 between different donors was noted. Analysis of lymphokine receptor mRNA demonstrated increased levels of mRNA for IL-2R alpha-chain and IFN-gamma receptor that preceded the phenotypic changes on the cell surface. In contrast, levels of IL-2R beta-chain and the TNF-alpha receptor mRNA decreased after stimulation. Amounts of IL-2, IL-4, and TNF-alpha, but not IFN-gamma, secreted also correlated with the levels of mRNA measured in the cells. Although costimulation through CD2, CD4, or LFA-1 appeared equally effective for the induction of the lymphokine receptors, these additional stimuli had a different impact on lymphokine secretion. These results indicate that specific control of lymphokine secretion and receptor induction can be another function of the CD2, CD4, and CD11a cell surface receptors. This control is evident at both transcriptional and post-transcriptional levels.

Antibodies↗
PubMed1977

Lymphokines of T and B cells. I. Demonstration that T and B cells of tumor antigensensitised mice produce different lymphokines changing surface charge of target cells.

Lymphocytes from MC sarcoma-bearing mice were exposed to a soluble tumor antigen. The lymphokine-containing supernatant thus obtained was fractionated on Sephadex G-75. Fractions were tested for their activity to reduce the surface charge of indicator macrophages by cell electrophoresis technique. When unseparated spleen or lymph node cells were used the charge-reducing activity of the supernatant was found in three regions according to molecular weights of about 100,000, 60,000 - 35,000 and 13,000 Daltons. The appearance of activity was found to be time-dependent. As indicated by tests with separated lymphocytes both B and T cells appear to release charge-reducing activity.

Animals↗
PubMed1992

Mechanism of interferon gamma-induced protection of human gliosarcoma cells from lymphokine-activated killer lysis: division of lymphokine-activated killer cells into natural killer- and T-like cells.

The mechanism by which interferon gamma (IFN-gamma) decreases the susceptibility of the established cultured gliosarcoma line Gl-1 to lymphokine-activated killer (LAK) lysis was analyzed. The results of monolayer depletion and lectin-dependent cellular cytotoxicity assays by LAK cells revealed that the resistance to LAK lysis of IFN-gamma-treated Gl-1 cells is manifested at the stage of LAK cell target recognition alone. We have also divided LAK cells into populations of phenotypically natural killer (NK)- and T-like cells with monoclonal antibodies and complement, respectively. We have used these cells to examine the mechanism of IFN-gamma-induced protection of Gl-1 cells from LAK lysis in cold target inhibition, monolayer depletion, and direct binding assays. The results revealed that NK-like cells do not recognize IFN-gamma-treated Gl-1 cells as efficiently as they do untreated targets, whereas T-like cells show the opposite tendency. In conclusion, we have demonstrated that the IFN-gamma induced protection of tumor cells from LAK lysis is predominantly regulated by the target recognition of NK-like cells. On the other hand, IFN-gamma-treated tumor cells may bind to T-like cells but fail to trigger them to initiate further stages for lysis as effectively as NK-like cells.

Cell Division↗
PubMed1976

Antibodies to guinea pig lymphokines. IV. Suppression of the mixed leukocyte culture reaction by anti-lymphokine globulin.

An antiserum, (anti-lymphokine globulin, ALyG) directed against highly purified products of activated lymphocytes, inhibits the proliferation of responding cells in guinea pig mixed leukocyte cultures ((MLC). This serum recognizes three newly synthesized lymphocyte products (one of them being migration inhibition factor (MIF) which are involved in the mediation of delayed hypersensitivity reactions in vivo. Since ALyG does not appear to contain cytotoxic antibodies against guinea pig lymphocyte antigens and its inhibitory activity cannot be removed by absorption with lymphoid cells it seems likely that the inhibition of MLC reactivity is not mediated by the lysis of stimulator or responder cells and its target is not the lymphocyte per se but possibly some factor elaborated during MLC response. By contrast, antisera with specificity for histocompatibility (H) antigens can inhibit the MLC when the appropriate H antigens are present on the responding and/or stimulating cell population. However, this inhibitory of the antisera can be effectively absorbed with lymphoid cells bearing the appropriate H antigens. The addition of ALyG even 48 hr after the initiation of culture results in a marked inhibition of MLC reactivity. This finding is consistent with the elaboration of a mitogenic factor or signal during the first 48 hr of culture and the delivery of this signal to the responding cell population. Thus, ALyG does not appear to interfere with the synthesis of this factor but must be present after its release in order to block responder cell proliferation. Furthermore, the stimulatory effect of this MLC mitogenic factor, but not of PPD-induced mitogenic factor on "third party" cells can be completely inhibited when the cells are cultured in the presence of ALyG. These findings suggest that the MLC-mitogenic factor in this system is identical to or cross-reactive with one or both of the newly synthesized molecules recognized by the ALyG.

Animals↗
PubMed1992

Regulation of lymphokine-activated killer cell induction by human recombinant IL-1 receptor antagonist. Obligate paracrine pathway of IL-1 during lymphokine-activated killer cell induction.

IL-2-stimulated human lymphocytes, referred to as lymphokine-activated killer (LAK) cells, can develop a broad range of lytic activity against fresh tumor cells and cultured tumor cell lines. IL-1, a pleiotropic cytokine shown to synergize with IL-2 on LAK induction, is endogenously synthesized and secreted by LAK cells. Immunoblot analysis demonstrated that IL-2-stimulated PBL produced the 31- to 34-kDa pro-molecules of IL-1 within 24 h and maintained their expression for at least 96 h. The role of secreted IL-1 has been examined using rIL-1R antagonist (IL-1ra). The addition of IL-1ra to LAK activation culture resulted in dose-dependent inhibited lytic activity, which was more apparent in LAK cells cultured with higher doses of IL-2. However, IL-1ra had no effect on proliferative responses elicited in LAK cells by IL-2. Moreover, when IL-1 binding was blocked by IL-1ra, the expression of the IL-2R p55 subunit was reduced compared with control LAK cells. The effect of IL-1 binding blockade on expression of other cytokine mRNA was further examined by polymerase chain reaction analysis, and, specifically, inhibition of both TNF-alpha and TNF-beta mRNA expression by IL-1ra was observed in PBL stimulated with IL-2. The reduced biologic activity of TNF in culture supernatants correlated well with the inhibition of mRNA expression. These findings suggest that autocrine/paracrine IL-1 is involved in the initial generation of LAK activity and, in particular, that TNF expression could be induced via an IL-1 autocrine pathway.

Base Sequence↗
PubMed1979

Biochemical and biological characterization of lymphocyte regulatory molecules. I. Purification of a class of murine lymphokines.

Murine spleen cells activated by concanavalin A (Con A) in culture produce a class of lymphokine molecules which possess biological activity in a number of lymphocyte response assays. Lymphokines with a mol wt of 30,000, as estimated from gel filtration studies, can be resolved into two components which differ by charge, with isoelectric point (pI) values of 4.3 and 4.9, respectively. Both components stimulate (a) the growth of established T-cell lines in culture, (b) the proliferation of thymocytes in the presence of Con A under culture conditions where Con A alone is nonmitogenic, (c) the induction of antibody responses to heterologous erythrocyte antigens in athymic (nude) spleen cultures, (d) the generation of cytotoxic T lymphocytes (CTL) in thymocyte cultures, and (e) the generation of CTL in nude spleen cultures. In each of these culture systems we suggest that the assays are detecting a single class of lymphokine which acts directly on activated T cells. Nonactivated T cells must be stimulated by either antigen or mitogen before becoming responsive to lymphokine, but do not require antigen or mitogen for continued growth with lymphokine. The two molecular species, separable by isoelectric focusing are referred to as the T-cell growth factor (TCGF). A lymphokine, similar in size (30,000 daltons) to TCGF but heterogeneous in charge (pI 3.0--4.0), stimulates immune responses to erythrocyte antigens in T-cell-depleted spleen cultures but has no stimulatory activity in the other lymphocyte assay systems described. The data have been interpreted as showing the two molecular forms of murine TCGF (pI 4.3 and 4.9) are responsible for many of the lymphokine activities described elsewhere as thymocyte mitogenic factor, nonspecific T-cell-replacing factor and killer helper factor or costimulator. The other lymphokine, separable from TCGF by charge, appears to have true T-cell-replacing activity.

Animals↗
PubMed1978

A comparison of the hematogenous cell infiltrate evoked by lymphokine injection with that of delayed hypersensitivity reactions.

Lymphokine preparations of high potency obtained by in vitro assay were employed in vivo to determine whether they could produce inflammatory responses showing a cellular infiltrate that qualitatively or quantitatively resembled responses of delayed hypersensitivity. Hematogenous cell infiltrates in guinea pig skin were characterized in terms of the number and types of participating cells following intradermal injection of either lymphokines or an antigen (PPD) to which the animals exhibited delayed hypersensitivity. The dose of lymphokine or PPD per skin test site was selected on the basis of comparable ability to enhance vascular permeability. Delayed hypersensitivity responses showed, as expected, a persistent mononuclear cell exudate both in dermis and subcutis, but most notable in the dermis, during the 24 hours following antigen injection. In contrast, the response to lymphokine over the same period was characteristically neutrophilic and principally in the subcutis. There was no pronounced mononuclear cell infiltrate at any time throughout the reaction to lymphokine. It is concluded that preformed lymphokine produces a pattern of increased vascular permeability appropriate to a mediator of delayed hypersensitivity reactions, provided there is sustained secretion of this material. The ability of lymphokine to cause carbon labeling of dermal capillaries is also pertinent to a mediator of delayed hypersensitivity. The absence of significant mononuclear cell accumulation suggests that the in vitro chemotactic activity of lymphokine toward mononuclear cells may be more important for retention of mononuclear cells in the extravascular connective tissue space than for their selective accumulation.

Animals↗
PubMed1992

Activation of lymphokine genes in T cells: role of cis-acting DNA elements that respond to T cell activation signals.

Activation of T cells is initiated by the recognition of antigen on antigen presenting cells to exert the effector functions in immune and inflammatory responses. Two types of helper T cell (Th) clones (Th1 and Th2) are defined on the basis of different patterns of cytokine (lymphokine) secretion. They determine the outcome of an antigenic response toward humoral or cell-mediated immunity. Although lymphokine genes are coordinately regulated upon antigen stimulation, they are regulated by the mechanisms common to all as well as those which are unique to each gene. For most lymphokine genes, a combination of phorbol esters (phorbol 12-myristate 13 acetate, PMA) and calcium ionophores (A23187) is required for their maximal induction. Yet phorbol ester alone or calcium ionophore alone produce several lymphokines. The production of the granulocyte-macrophage colony stimulating factor (GM-CSF) is completely dependent on the two signals. We have previously found a cis-acting region spanning the GM-CSF promoter region (positions -95 to +27) that confers inducibility to reporter genes in transient transfection assays. Further analysis identified three elements required for efficient induction, referred to as GM2, GC-box and conserved lymphokine element (CLE0). GM2 defines a binding site for protein(s) whose binding is inducible by PMA. One protein, NF-GM2 is similar to the transcription factor NF-kB. GC-box is a binding site for constitutively bound proteins. CLEO defines a binding site for protein(s) whose optimum binding is stimulated by PMA and A23187. Viral trans-activators such as Tax (human T cell leukemia virus-1, HTLV-1) and E2 (bovine papilloma virus, BPV) proteins are other agents which activate lymphokine gene expression by bypassing T cell receptor (TCR) mediated signaling. The trans-activation domain of E2 and Tax is interchangeable although they have no obvious sequence homology between them. The viral trans-activators appear to target specific DNA binding protein such as NF-kB and Sp1 to cis-acting DNA site and promote lymphokine gene expression without TCR-mediated stimulation.

Animals↗
PubMed1992

Hyper-IgM immunodeficiency syndrome: influence of lymphokines on in vitro maturation of peripheral B cells.

Peripheral B cells from six patients affected with the hyper-IgM immunodeficiency syndrome, characterized by an absence of IgG and IgA in serum with a concomitant elevated level of IgM, were analyzed for phenotypic and functional characteristics. We report that although the membrane antigenic pattern expression was characteristic of mature B cells, B cells from most patients exhibited an impairment in their in vitro response to several lymphokines, such as recombinant interleukin 2 (rIL-2) and low molecular weight B-cell growth factor (BCGF), that induce proliferation of anti-mu-activated B cells. This impairment was also found in response to a lymphokine mixture from a CD2-activated T-cell clone. The decrease in lymphokine-induced B-cell proliferation was accompanied by a low B-cell differentiation, whether patients' B cells were stimulated by the T-cell clone supernatant or rIL-2 and rIL6, lymphokines able to support differentiation of Staphylococcus aureus Cowan I (SAC)-activated B cells. In addition, none of the lymphokines tested were able to induce patients' B cells to switch from IgM-secreting cells to IgG- and IgA-secreting cells. We conclude that this syndrome is associated with a defect in lymphokine-dependent maturation of B lymphocytes, although the T- or the B-cell origin of the defect still cannot be determined.

Antibody-Producing Cells↗
PubMed1979

Aspects of cellular immunity in multiple sclerosis. Antigen-reactivity of lymphocytes and lymphokine activity.

Some new results of cell-mediated immunity in multiple slcerosis (MS) are presented, based on the determination of charge-changing lymphokines as products of antigen sensitive lymphocytes (C PAL), obtained by several forms of the electrophoretic mobility (EM) method. Lymphocytes from MS react to myelin basic protein (BP), the reactivity in other neurological diseases depending on the degree of destruction of nervous parenchyma. Applying a membrane-associated antigen from normal brain (NTA), positive reactivity of MS lymphocytes was obtained. Besides the usual determination of lymphokines in vitro the sensitive EM test allows the demonstration of lymphokine activities in vivo; i.e. in body fluids such as cerebrospinal fluid (CSF) and serum. In CSF of MS a high lymphokine activity was found. The differentiation of lymphokines and comparison between in vitro and in vivo activity were carried out. Moreover, a characteristic lymphokine pattern for MS with high activities in all regions of molecular weight, especially in the CSF, could be detected. On the basis of these findings, important also from the pathogenetic point of view, a diagnostic scheme for MS is suggested, consisting of a program of determination of the immuno-reactive CSF syndrome and some special procedures, including examination of lymphocyte reactivity.

Brain↗
PubMed1975

Studies on the contact sensitization of man with simple chemicals. III. Quantitative relationships between specific lymphocyte transformation, skin sensitivity, and lymphokine activity in response to dinitrochlorobenzene.

Dinitrochlorobenzene (DNCB) coupled to peripheral blood erythrocytes or leukocytes forms a particulate complex, DNCB-antigen. The addition of DNCB-antigen induced blastogenesis and DNA synthesis in leukocyte cultures from DNCB-sensitized human subjects and not in leukocyte cultures from nonsensitized controls. In general, sensitized subjects who displayed a higher degree of cutaneous reactivity to DNCB, as manifested by duration and intensity of dermatitis, also showed a greater blastogenic response to DNCB-antigen in vitro. This quantitative correlation, however, was not invariant. Certain soluble factor(s), or lymphokines are released following the addition of DNCB-antigen to leukocyte cultures prepared from some sensitive subjects who were rechallenged one or more times with DNCB. These lymphokines induce blastogenesis in secondary target leukocyte populations from nonsensitized subjects. Extended studies are presented which slow little or no lymphokine activity in peripheral blood leukocyte cultures during a primary immune response, despite high degrees of blastogenic activity in response to DNCB-antigen. Significant lymphokine activity was observed only following additional rechallenge with DNCB. Blastogenesis and skin reactivity specific for DNCB have been shown to develop at about the same time during a primary immune response. This, along with the quantitative correlation shown in this communication, suggests that both processes probably reflect thymic-dependent cellular immunity. The appearance of lymphokine activity following rechallenge with DNCB suggests that DNCB-induced lymphokines may represent an amplifying mechanism of the cellular immune response that involves recruitment of previously uncommitted lymphocytes.

Antigens↗
PubMed1992

Qualitative shift of lymphokine production in response to stimulation, as a consequence of preactivation in vivo or in vitro.

Lymphokine production, analysed at the single cell level, was compared in resting and primed T-cell populations. Cells were preactivated in vitro by repeated mitogen stimulations, or isolated as large, low density cells naturally activated in vivo, from normal spleens of unimmunized animals. A similar qualitative shift in the pattern of lymphokines synthesized after restimulation was found as a result of in vivo and in vitro preactivation of cells. Repeated stimulations in vitro resulted in a qualitative shift in the lymphokines produced in response to activation, from a dominance of IL-2 during the first and second culture, to a dominance of IL-4 and IL-5 in the later stimulations. In vivo activation lead to a similar separation of lymphokine production as primarily IL-2 was made by small resting cells, while large cells preferentially produced IL-4 and IL-5. IFN-gamma was produced by both small and large cells. Preactivation in vitro lead to a more rapid appearance of lymphokines during restimulation. In contrast, the in vivo naturally activated cells responded with a slow onset of lymphokine production when stimulated in vitro.

Animals↗
PubMed1976

Administration of peripheral-blood rat-lymphocytes stimulated "in vitro" with human lymphokines and spleen colonies in the total body irradiated rat.

It was previously reported that PHA-incubation of a pool of peripheral-blood lymphocytes before their i.v. injection into rats submitted to total body irradiation, stimulates spleen colony formation and growth. On the same model, the present study has investigated the effect of lymphocyte preincubation with supernates obtained in short term cultures from human lymphocytes prestimulated with PHA (lymphokines). The "in vitro" culture of rat lymphocytes in a medium supplemented with human lymphokines showed either a marked increase of lymphocyte survival rate, or significant stimulation of lymphocyte blastogenesis, but at an extent much lower than that caused by PHA, also because in this particular experiment the culture medium was supplemented with too little amount of lymphokines. These data support the interpretation that human lymphokines may act across the species barriers. Peripheral-blood rat lymphocytes prestimulated with human lymphokines, and then injected i.v. into rats previously submitted to total body irradiation, caused significant increase in the spleen weight, as well as formation of spleen colonies quite larger and with higher erythroid differentiation - though less numerous than in the controls (i.e., in the rats injected just with untreated lymphocytes). This behaviour may be due to the tendency to merge together of two or more colonies in a single giant colony, and supports the interpretation that immune-competent lymphocytes activated either with PHA or with lymphokines may stimulate spleen colony growth and erythroid differentiation, though at different extents.

Animals↗
PubMed1992

Retroviral vector-mediated lymphokine gene transfer into human renal cancer cells.

Effective vaccination against cancer, either for prophylaxis or therapy, has been an elusive goal for years. Cytokine gene therapy offers a novel approach to generate immunogenic tumor cell vaccines. To examine the feasibility of cytokine gene transfer into human renal cancer (RC) cells, we introduced the cDNAs for human interleukin-2 (IL-2) or interferon-gamma (IFN-gamma) into various RC cell lines with retroviral vectors. Using the NIH3T3 amplification assay, no replication competent retroviral particles were detectable in cell culture supernatants taken from gene-modified RC cell lines. Efficient expression of both lymphokines was achieved. Depending on the cell line and the vector construct used, lymphokine gene-modified human RC cell lines released 4 to 29 units/10(6) cells of IL-2, or up to 10 units/10(6) cells of IFN-gamma within 48 h. Fluorescence-activated cell sorter analysis of SK-RC-29 cells releasing IFN-gamma showed increased expression of major histocompatibility complex class I antigen, beta 2-microglobulin, and ICAM-1, as well as induction of major histocompatibility complex class II antigen expression [human leukocyte antigen(HLA)-DR, -DP], but no changes in these cell surface markers were observed with SK-RC-29 cells releasing IL-2. Following in vitro gamma-irradiation with 5,000 or 10,000 rad, growth of lymphokine gene-modified RC cells was abrogated, but their capability to release lymphokine and express lymphokine-induced antigenic determinants, such as HLA-DR, was retained. Tumor formation by the human RC cell line SK-RC-29 in BALB/c nude mice was not affected by IFN-gamma secretion, but was inhibited by in vivo release of IL-2 from s.c. injected tumor cells. These studies demonstrate the feasibility of retroviral mediated lymphokine-gene transfer into human RC cells and suggest a means for generating autologous or HLA-matched allogeneic tumor cell vaccines for the treatment of patients with renal cell carcinoma.

Animals↗
PubMed1977

Leucocyte chemotactic activity in the parallel bioassay of guinea--pig lymphokines.

This paper describes the application of parallel bioassay to determine the extent to which the leucocyte chemotactic activity of guinea-pig lymphokine preparations is associated with their lymphocyte mitogenic, inflammatory (increased vascular permeability) and macrophage migration inhibitory activities. A convenient test of chemotactic activity was devised whereby Coulter counter determinations were made of the number of peritoneal exudate cells passing through a Nuclepore membrane into the medium of the lower (test) compartment of a chemotaxis chamber. Symmetrical parallel line (2+2) dose assays were used to obtain potency ratio estimates of the chemotactic activity of seven lymphokine preparations whose mitogenic, inflammatory and migration inhibitory activities were already known. Statistical analysis of the results revealed a clear dissociation of chemotactic activity from mitogenic and migration inhibitory activities; but with six of the seven lymphokine preparations, a marked similarity was revealed between their chemotactic and inflammatory activities. Cytological studies showed that although the lymphokine preparations were chemotactic for different cell types, there was a preferential migration of neutrophils and the smaller mononuclear cells. The demonstration by parallel bioassay of an association between the ability of lymphokine preparations to increase vascular permeability in vivo and to promote chemotaxis of leucocytes in vitro is viewed in relation to the possible role of lymphokine in inflammatory processes.

Animals↗