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D G Colley - One of the best experts on this subject based on the ideXlab platform.
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in vivo molecular analysis of Lymphokines involved in the murine immune response during schistosoma mansoni infection ii quantification of il 4 mrna ifn gamma mrna and il 2 mrna levels in the granulomatous livers mesenteric lymph nodes and spleens du
Journal of Immunology, 1992Co-Authors: G S Henderson, T L Mccurley, D G ColleyAbstract:Parasite egg-induced granulomas are the primary pathogenic lesions in murine schistosomiasis mansoni. This cell-mediated granulomatous response is specific for soluble egg Ag and appears to be mediated predominantly by CD4+ Th2 cells. As infection progresses from the acute to the chronic phase, the cell-mediated anti-soluble egg Ag responses attenuate in a process termed modulation. In this study the hypothesis that modulation is effected by a chronic phase increase in Th2-inhibiting Th1 cell activity was investigated. Northern blot quantification of mRNA specific for the Th2 lymphokine, IL-4, and the Th1 Lymphokines, IFN-gamma and IL-2, in the spleens, mesenteric lymph nodes, and granulomatous livers of mice infected for various lengths of time over the course of modulation was performed. Also, the capacity of mitogen- and Ag-stimulated spleen cells to produce message for these Lymphokines was compared. Peak tissue levels of both IL-4 mRNA and IFN-gamma mRNA were seen in acutely infected mice, and levels of both messages declined as infection became chronic. Stimulated spleen cells from acutely infected mice also produced higher levels of IL-4 and IFN-gamma mRNA than cells from chronically infected mice. IL-2 mRNA was never detected in any tissue sample but was detected in the stimulated spleen cells, again with acute phase levels higher than chronic phase levels. Hence, this study shows no evidence for increased Th1 cell activity during chronic infection and suggests that modulation may be effected by a generalized suppression of lymphokine synthesis.
Michael H. Kogut - One of the best experts on this subject based on the ideXlab platform.
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longevity of augmented phagocytic activity of heterophils in neonatal chickens following administration of salmonella enteritidis immune Lymphokines to chickens
Avian Pathology, 2000Co-Authors: L L Genovese, Michael H. Kogut, Virginia K Lowry, K J GenoveseAbstract:Previously, our laboratory reported an existing relationship between ontogenesis of heterophil activity and susceptibility to Salmonella enteritidis infection in poultry during the first week post-hatch. The prophylactic administration of S. enteritidis-immune Lymphokines has been shown to enhance heterophil function in vitro and reduce S. enteritidis organ invasion in 1-day-old chicks. However, how long the heterophils remain activated is currently unknown. The objective of this research was to evaluate the duration of enhanced heterophil phagocytosis of S. enteritidis following the prophylactic administration of a single injection of S. enteritidis-immune Lymphokines to neonatal chicks. Administration of S. enteritidis-immune Lymphokines on the day of hatch resulted in a significant increase in heterophil phagocytic activity (P < 0.05) through day 5 post-hatch. No significant differences in phagocytic activities of heterophils from control and S. enteritidis-immune lymphokinetreated chicks was demonstrated from day 6 to 14 post-hatch. These data suggest that the administration of S. enteritidis-immune Lymphokines on day of hatch potentiates heterophil phagocytic activity during a critical period of susceptibility to Salmonella infection in neonatal chicks. The immune lymphokine-induced enhancement of heterophil activity subsides by day 5 as the chick's natural defenses mature and are able to resist infections without exogenous augmentation.
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ontogeny of the phagocytic and bactericidal activities of turkey heterophils and their potentiation by salmonella enteritidis immune Lymphokines
Fems Immunology and Medical Microbiology, 1997Co-Authors: Michael H. Kogut, Virginia K Lowry, K J Genovese, Lacy L BowdenAbstract:Heterophils, the functional equivalent to the mammalian neutrophil, are important mediators of natural resistance against invasive pathogens in poultry. Young poultry are susceptible to pathogens, such as Salmonella enteritidis, during the first week post-hatch. No studies have evaluated the ontogeny of heterophil function in turkeys during the first few weeks post-hatch. Previous studies from our laboratory have shown day-old poults were protected against S. enteritidis organ invasion following immunoprophylactic administration of chicken S. enteritids immune Lymphokines. Therefore, the objective in the present study was to characterize the development of phagocytosis and bacterial killing by turkey heterophils during the first 3 weeks of life and to compare the effect of immune Lymphokines on the development of heterophil phagocytosis and killing during the first 3 weeks post-hatch. Both functional phagocytosis and killing activities were age-dependent events. During the first 1–7 days post-hatch, little functional activity was demonstrated which apparently is associated with susceptibility. Optimal heterophil phagocytosis and killing activities were reached 14–21 days post-hatch. Administrating immune Lymphokines significantly potentiated phagocytosis (P<0.01) and killing (P<0.001) by turkey heterophils. In fact, immune lymphokine administration to 1–7-day-old poults augmented phagocytosis and killing activities of heterophils equivalent to levels found in functionally mature 14–21-day-old poults. These results demonstrate the ontogeny of the functional activity of the turkey heterophil is an age-related phenomenon, with inefficient phagocytosis and killing during the first week post-hatch. Prophylactic administration of immune Lymphokines significantly potentiated the functional activity of the heterophil from poults during the first 3 weeks of life. Most importantly the administration of immune Lymphokines enhanced the functional activity of heterophils from 1–7-day-old poults to levels comparable to that of an immunologically mature bird.
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immunoprophylaxis of salmonella enteritidis infection by Lymphokines in leghorn chicks
Avian Diseases, 1993Co-Authors: G Tellez, Michael H. Kogut, B M HargisAbstract:SUMMARY. Chickens were treated prophylactically with the soluble products from Con A-stimulated T-lymphocytes from Salmonella enteritidis-infected chickens in order to investigate the effect of such prophylactic treatment on organ invasion by S. enteritidis. At 18 days of age, chicks were injected intraperitoneally with one of the following: A) the Amicon YM 10 ultrafiltrate from immunized chickens, B) the Amicon YM 10 ultraretentate material from immunized chickens, or C) the Amicon YM 10 ultraretentate material from control nonimmune chickens. Thirty minutes after lymphokine injection, all birds were challenged per os with 108 colony-forming units of S. enteritidis. At both 1 and 6 days post-challenge, prophylactic treatment of chickens with the immune retentate resulted in a 51-60% reduction in S. enteritidis organ invasion. The reduction in S. enteritidis organ invasion was associated with a significant increase in lamina propria thickness based on morphometric analysis (P < 0.05). These results demonstrate that the prophylactic administration of S. enteritidis-immune Lymphokines induces protection against S. enteritidis organ invasion, which is associated with a measurable microanatomical change in the cecal mucosa.
Hermann Wagner - One of the best experts on this subject based on the ideXlab platform.
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differential effects of the immunosuppressive agents cyclosporine and leflunomide in vivo leflunomide blocks clonal t cell expansion yet allows production of Lymphokines and manifestation of t cell mediated shock
Transplantation, 1995Co-Authors: Roland Lang, Hermann Wagner, Klaus HeegAbstract:The effects of leflunomide and CsA on immune responses in vitro and in vivo were investigated. Like CsA, leflunomide inhibited mitogen- or antigen-driven T cell proliferation in vitro. However, leflunomide impaired neither the capability of T cells to produce IL-2 and IL-4, nor the expression of IL-2R, that is, the acquisition of competence. In contrast to CsA, the IL-2-driven growth of secondary T cells was blocked by leflunomide. Cell cycle analyses revealed that activated T cells did not enter S phase of the cell cycle in the presence of leflunomide. Next, the effects of leflunomide and CsA on the T cell response toward the bacterial superantigen (SAg) staphylococcal enterotoxin B (SEB) were analyzed in vivo. SEB-induced early deletion (apoptosis) of a fraction of SEB-reactive V beta 8+ T cells and IL-2R expression were not impaired by either CsA nor leflunomide. On the other hand, both CsA and leflunomide prevented V beta 8-selective clonal T cell expansion and generation of SEB-specific cytolytic activity. In contrast to CsA, leflunomide treatment permitted in vivo SEB-induced production of T cell-derived Lymphokines (IL-2 and TNF). Further, leflunomide failed to protect D-galactosamine-sensitized mice from SEB-induced, T cell-mediated lethal shock, whereas CsA was fully protective. Manifestation of SEB-induced T cell anergy was not impaired by leflunomide. Our results provide evidence that CsA and leflunomide differ significantly in their functional properties to suppress immune responses in that both agents inhibit T cell functions linked to clonal expansion, while leflunomide does not inhibit lymphokine secretion and thus permits lymphokine-mediated immune functions.
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t cell mediated lethal shock triggered in mice by the superantigen staphylococcal enterotoxin b critical role of tumor necrosis factor
Journal of Experimental Medicine, 1992Co-Authors: Thomas Miethke, Claudia Wahl, Klaus Heeg, Bernd Echtenacher, Peter H Krammer, Hermann WagnerAbstract:Because mice are more resistant than humans to the pathogenic effects of bacterial toxins, we used D-Galactosamine- (D-Gal) sensitized mice as a model system to evaluate potential toxic shock symptoms triggered by the superantigen staphylococcal enterotoxin B (SEB). We show that similar to endotoxin (lipopolysaccharide) [LPS], the exotoxin SEB causes lethal shock within 8 h in D-Gal-sensitized mice, inducing 100% and about 50% lethality with 20 and 2 micrograms SEB, respectively. The lethal shock triggered by the superantigen SEB is mediated by T cells, a conclusion based on the observation that T cell repopulation of SCID mice conferred sensitivity to SEB. Since CSA also conferred protection, the role of T cell-derived Lymphokines in mediating lethal shock was evaluated. Within 30-60 min after SEB injection, serum tumor necrosis factor (TNF) levels peaked, followed immediately by interleukin-2 (IL-2). Serum-borne Lymphokines were detected well in advance of signs of T cell activation, as assessed by IL-2 receptor expression of SEB-reactive V beta 8+ T cells. Passive immunization with anti-TNF-alpha/beta-neutralizing monoclonal antibody also conferred protection, indicating that it is TNF which is critical for initiating toxic shock symptoms. Taken together, this study defines basic differences between endotoxin (LPS)- and exotoxin (SEB)-mediated lethal shock, in that the former is mediated by macrophages and the latter by T cells. Yet the pathogenesis distal to the lymphokine/cytokine-producing cells appears surprisingly similar in that TNF represents a key mediator in inducing shock.
Susan L Swain - One of the best experts on this subject based on the ideXlab platform.
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Characterization of Antigen-specific CD4+ Effector T Cells In Vivo: Immunization Results in a Transient Population of MEh14-, CD45RB- Helper Cells that
2013Co-Authors: Interferon Y, S Tonkonogy, D D Duncan, M Bradley, Susan L SwainAbstract:In previous studies we demonstrated that, following activation by mitogens or alloantigens, helper T cell precursors proliferate and differentiate in vitro to produce a population of effector cells that secrete high titers of Lymphokines upon restimulation. In this report, we demonstrate that a similar effector population develops in vivo following primary antigen stimulation. When restimulated with specific antigen in vitro, CD4+ T cells from mice primed 5 to 7 days previously by subcutaneous administration of keyhole limpet hemocyanin (KLH) in adjuvant, produced high levels of interleukin 2 (IL2), IL4, and IL 3, and little or no interferon y (IFN-'y) or IL-5. The effector T cells provided excellent helper activity for in vitro antibody responses of 4-hydroxy-5-iodo-nitrophenyl acetic acid-primed B cells with the production principally of the immunoglobulin Gt (IgGI) and IgM isotypes, small quantities of IgG3, and no detectable IgG2a, or IgG2b. Antigen-specific secretion of 11,2, IL-3, and ILA by in vivo effectors was detectable by 12 hours following in vitro restimulation. IFN-y and IL5 were not detected until 48 and 72 hours of culture, respectively, and low levels of these Lymphokines were produced. Lymphokine production by primed CD4+ T cells could be induced as early as 3 days following immunization, peaked on day 5, and declined thereafter. The kinetics of in vivo appearance of effector CD4
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helper t cell subsets phenotype function and the role of Lymphokines in regulating their development
Immunological Reviews, 1991Co-Authors: Susan L Swain, Linda M Bradley, D D Duncan, Michael Croft, Susan L Tonkonogy, Gus Atkins, Andrew D Weinberg, Stephen M Hedrick, Richard W Dutton, Gail E HustonAbstract:We have concentrated here on the Lymphokines which might serve to regulate the different pathways of precursor development. We suggest that, as a result of antigenic stimulation, specific precursor cells both proliferate and become committed to develop into either an effector cell, a memory cell or an anergized cell. Anergy has not been dealt with in this review, but it is likely to be one of the options available. The development of an effector population takes 4-7 d (quite analogous to the time it takes for CTLp to become CTL and for resting B to become Ab-forming cells). The effector populations are large, generally IL-2R-positive cells. These cells have upregulated many adhesion molecule systems [e.g., Pgp-1, LFA-1 and ICAM-1 (Swain unpublished)], but downregulated the Mel-14 homing receptor. Effectors are ready to respond to APC such as specific B cells with a rapid synthesis and secretion of Lymphokines. The effector population is then quickly downregulated, both by the turn off of lymphokine synthesis/secretion and possibly by its own suicide. This kind of pattern makes teleological sense since the cells making such high titers of Lymphokines could have many potent pleitropic effects. It also seems to be the strategy employed in the generation of other terminally differentiated effectors (such as CTL and plasma cells). The requirement for restimulation and the requirement for direct and perhaps prolonged contact between the helper effector and the APC-B cell can be expected to help ensure that these Lymphokines are localized (reviewed in Swain & Dutton 1987, Swain & Croft 1990) and effectively delivered to specific responding cells. We postulate that at the same time, or perhaps subsequent to this, another set of signals drives precursors to generate prememory cells. Our studies suggest these emerging memory cells may be phenotypically unique and we postulate that they are specialized to become a "long-lived" population of memory cells that will persist indefinitely as a protective population of increased frequency for the antigen encountered and which is also able to respond more rapidly and effectively. The greater effectiveness of the memory response would thus be due to dramatically increased frequency, to characteristic and stable changes in adhesion molecule expression and to the fact that, in addition to IL-2, resting memory cells also secrete at least low titers of IL-3, IL-4, IFN-gamma and other Lymphokines upon initial restimulation.(ABSTRACT TRUNCATED AT 400 WORDS)
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characterization of antigen specific cd4 effector t cells in vivo immunization results in a transient population of mel 14 cd45rb helper cells that secretes interleukin 2 il 2 il 3 il 4 and interferon gamma
Journal of Experimental Medicine, 1991Co-Authors: Linda M Bradley, D D Duncan, S Tonkonogy, Susan L SwainAbstract:In previous studies we demonstrated that, following activation by mitogens or alloantigens, helper T cell precursors proliferate and differentiate in vitro to produce a population of effector cells that secrete high titers of Lymphokines upon restimulation. In this report, we demonstrate that a similar effector population develops in vivo following primary antigen stimulation. When restimulated with specific antigen in vitro, CD4+ T cells from mice primed 5 to 7 days previously by subcutaneous administration of keyhole limpet hemocyanin (KLH) in adjuvant, produced high levels of interleukin 2 (IL-2), IL-4, and IL-3, and little or no interferon gamma (IFN-gamma) or IL-5. The effector T cells provided excellent helper activity for in vitro antibody responses of 4-hydroxy-5-iodo-nitrophenyl acetic acid-primed B cells with the production principally of the immunoglobulin G1 (IgG1) and IgM isotypes, small quantities of IgG3, and no detectable IgG2a, or IgG2b. Antigen-specific secretion of IL-2, IL-3, and IL-4 by in vivo effectors was detectable by 12 hours following in vitro restimulation. IFN-gamma and IL-5 were not detected until 48 and 72 hours of culture, respectively, and low levels of these Lymphokines were produced. Lymphokine production by primed CD4+ T cells could be induced as early as 3 days following immunization, peaked on day 5, and declined thereafter. The kinetics of in vivo appearance of effector CD4+ T cells that produce Lymphokines upon restimulation in vitro were similar for each of the Lymphokines examined. Mice depleted of precursor CD4+ T cells by adult thymectomy exhibited limited capacity to generate lymphokine secreting CD4+ T cells in response to primary immunization with KLH, suggesting that the majority of lymphokine producing T cells arise from short-lived and/or precursor cells. Separation of CD4+ T cells from KLH-primed mice on the basis of expression of the lymph node-specific homing receptor, MEL-14, revealed that antigen-specific production of IL-2, IL-3, IL-4, and IFN-gamma was exclusively associated with the MEL-14- subset of CD4+ T cells. Separation on the basis of CD45RB expression, demonstrated that antigen-specific lymphokine production was primarily associated with the minor CD45RB- population, which has been previously associated with memory activity. Our results indicate that primary in vivo immunization leads to the development of a transient population of helper-effectors with a unique phenotype that can produce large quantities of Lymphokines and mediate excellent helper activity for B cells.(ABSTRACT TRUNCATED AT 400 WORDS)
G S Henderson - One of the best experts on this subject based on the ideXlab platform.
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in vivo molecular analysis of Lymphokines involved in the murine immune response during schistosoma mansoni infection ii quantification of il 4 mrna ifn gamma mrna and il 2 mrna levels in the granulomatous livers mesenteric lymph nodes and spleens du
Journal of Immunology, 1992Co-Authors: G S Henderson, T L Mccurley, D G ColleyAbstract:Parasite egg-induced granulomas are the primary pathogenic lesions in murine schistosomiasis mansoni. This cell-mediated granulomatous response is specific for soluble egg Ag and appears to be mediated predominantly by CD4+ Th2 cells. As infection progresses from the acute to the chronic phase, the cell-mediated anti-soluble egg Ag responses attenuate in a process termed modulation. In this study the hypothesis that modulation is effected by a chronic phase increase in Th2-inhibiting Th1 cell activity was investigated. Northern blot quantification of mRNA specific for the Th2 lymphokine, IL-4, and the Th1 Lymphokines, IFN-gamma and IL-2, in the spleens, mesenteric lymph nodes, and granulomatous livers of mice infected for various lengths of time over the course of modulation was performed. Also, the capacity of mitogen- and Ag-stimulated spleen cells to produce message for these Lymphokines was compared. Peak tissue levels of both IL-4 mRNA and IFN-gamma mRNA were seen in acutely infected mice, and levels of both messages declined as infection became chronic. Stimulated spleen cells from acutely infected mice also produced higher levels of IL-4 and IFN-gamma mRNA than cells from chronically infected mice. IL-2 mRNA was never detected in any tissue sample but was detected in the stimulated spleen cells, again with acute phase levels higher than chronic phase levels. Hence, this study shows no evidence for increased Th1 cell activity during chronic infection and suggests that modulation may be effected by a generalized suppression of lymphokine synthesis.
