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At least 55 records · Page 3Linked to original sources
PubMed1976

Host immune responses after administration of inactivated Venezuelan equine encephalomyelitis virus vaccines. I. Description and characterization of adoptive transfer by immune spleen cells.

Cellular immune responses after immunization with a number of inactivated Venezuelan equine encephalomyelitis (VEE) virus vaccines were evaluated in mice by means of an adoptive transfer system. Formalin-inactivated, TC-83 strain VEE virus vaccine was immunogenic and highly effective in protecting recipient mice against challenge with virulent VEE virus. In contrast to immunization with live TC-83 VEE virus vaccine, however, immunization with inactivated VEE vaccine did not provide donor mice with the capacity to transfer adoptive immunity readily. Only when mice were immunized with inactivated VEE vaccine combined with specific adjuvants (particularly complete Freund's adjuvant or Bordetella pertussis) were donors capable of consistently transferring adoptive immunity. The total dose of inactivated VEE vaccine did not appear to influence the capacity to transfer adoptive immunity. On the other hand, weekly boosters of VEE vaccine and/or administration of vaccine with specific adjuvants did markedly influence donor immune responses.

Animals↗
PubMed1978

Significance of thymus-derived lymphocytes in immunity elicited by immunization with ribosomes or live yeast cells of Histoplasma capsulatum.

The lymphoid cells responsible for protective immunity to histoplasmosis were characterized. Adoptive transfer of spleen and peritoneal cells treated with antiserum to theta-antigen from mice immunized with ribosomes or live yeast cells of Histoplasma capsulatum abrogated the ability of these cells to protect the syngeneic recipients, whereas treatment of lymphoid cells with antiserum to IgG did not affect the immunity. Prior removal of glass-adhering cells from spleen and peritoneal cell suspensions did not alter their protective activity. Treatment with mitomycin C, an antimitotic agent, ablated the capacity of immune lymphocytes to protect the syngeneic recipients. These results indicate that the immune spleen and peritoneal cells that confer immunity to histoplasmosis are thymus-dependent (T) lymphocytes and that their active proliferation in the recipients is necessary for expression of the protective immunity. Furthermore, the immunity elicited by immunization with histoplasma ribosomes and live yeast cells is mediated by a similar mechanism.

Adhesiveness↗
PubMed1979

Passive-active immunity from hepatitis B immune globulin. Reanalysis of a Veterans Administration cooperative study of needle-stick hepatitis. The Veterans Administration Cooperative Study Group.

The mechanism of action of hepatitis B immune globulin (HBIG) and immune serum globulin was sought in a reanalysis of a Veterans Administration cooperative study on needle-stick exposure to hepatitis B surface antigen (HBsAg)-positive blood. Sera from 296 exposed persons were tested for HBsAg, antibody to HBsAg (anti-HBs), and antibody to hepatitis B core antigen (anti-HBc) by radioimmunoassay. Type B hepatitis developed in three HBIG (2%) and in 12 ISG (8%) recipients. In contrast, subclinical infection (development of HBsAg or anti-HBs and anti-HBc without symptoms or jaundice) developed in 16 HBIG (10%) but only six immune serum globulin (4%) recipients. Thus, infection occurred equally in both groups but was more likely to be subclinical in HBIG recipients, indicating that HBIG permitted development of passive-active immunity to type B hepatitis. An additional 53 immune serum globulin recipients (36%) but only one HBIG recipient developed anti-HBs alone, without hepatitis, HBsAg, or anti-HBc. This response was more compatible with immunization by HBsAg than with infection. Ultracentrifugation analysis revealed occult HBsAg in the immune serum globulin but not the HBIG, indicating that some immune serum globulin preparations contain HBsAg and can induce active immunity to type B hepatitis.

Hepatitis B↗
PubMed1975

Inhibition of the cellular immune response to simian virus 40 tumor cells in tumor-bearing and tumor-immune mice by concanavalin A.

The effects of in vivo-administered concanavalin A (Con A) on the kinetics of the primary and secondary cellular immune responses to simian virus 40-transformed tumor cells were investigated in BALB/c mice. Either a single initial dose of 400 mug Con A or daily doses of 50 mug depressed the cell-mediated immune response to tumor cells during the progressive growth of tumors, as determined by a radioisotopic foot-pad assay. The immune depression correlated with an increase in ultimate tumor weight. Similarly, Con A suppressed the antitumor cellular immune response in tumor-immune animals. Immune reactivity returned within 6 days after a single injection of 400 mug Con. Continuous administration 50 mug Con A resulted in a gradual decline in antitumor cellular immune responsiveness, which reached a plateau by the 5th day. Splenic lymphocytes from Con A-treated, immune mice failed to elicit a local adoptive transfer reaction; their immune responsiveness tended to return after incubation with alpha-methyl-D-pyranosyl sugars.

Animals↗
PubMed1977

Passive transfer of systemic tumor immunity with cells generated in vitro by a secondary immune response to a syngeneic rat gross virus-induced lymphoma.

Spleen cells taken from W/Fu rats 4 to 6 weeks after immunization with the syngeneic Gross virus-induced lymphoma, (C58NT)D cells, at a time when they lack detectable activity in a short-term 51Cr release assay, were previously shown to retain the capacity to generate cytotoxic activity upon reexposure to mitomycin C-treated lymphoma (C58NT)D cells in vitro. In the studies presented here, we evaluated whether in vitro sensitization of immune lymphoid cells before systemic transfer to a nonimmune recipient allows for more effective transfer of tumor immunity. The results show that the passive transfer of immune spleen cells after in vitro cocultivation with mitomycin-treated (C58NT)D cells allows for inhibition of growth of a subcutaneous inoculum of lymphoma cells. In contrast, spleen cells obtained 4 to 6 weeks after primary sensitization or after secondary in vivo sensitization did not effectively confer anti-tumor immunity. As few as 5 x 107 in vitro sensitized cells permitted complete inhibition of 106 (C58NT)D cells and also allowed for inhibition of the growth of 107 (C58NT)D-F cells, which was lethal to control animals. Immune cells sensitized with syngeneic thymocytes or normal spleen cells sensitized with (C58NT)D cells in vitro did not confer in vivo anti-tumor immunity. After systemic transfer of in vitro sensitized cells, delayed hypersensitivity occurred at the site of tumor inoculation and tumor growth was suppressed. Specificity of the passive immunity was shown by the failure to inhibit growth of a polyoma virus-induced sarcoma in rats which inhibited growth of the Gross virus-induced lymphoma cells. In vitro sensitized cells were more effective in the transfer of anti-tumor protection after 5 days, as compared to 2 days, of cocultivation with tumor. Results show that in vitro sensitized cells can effectively transfer systemic tumor immunity.

AKR murine leukemia virus↗
PubMed1977

Specificity of antitumor immune reactions mediated by xenogeneic immune RNA.

Evidence that xenogeneic immune RNA (I-RNA) mediated specific cytotoxic immune responses against human tumor-associated antigens was obtained from in vitro studies in two autologous melanoma systems. In these systems, malignant melanoma target cells, matching normal fibroblast target cells, lymphocyte effector cells, and melanoma and normal skin tissue used to immunize RNA donor animals were derived from the same autochthonous hosts. When incubated with autologous lymphocytes, I-RNA extracted from the lymphoid organs of donor animals immunized with melanoma tissue mediated immune reactions against autologous melanoma target cells in vitro. I-RNA from animals immunized with normal skin tissue from autochthonous hosts did not increase the cytotoxicity of autologous lymphocytes for autologous melanoma cells. Using autologous fibroblasts as target cells, we detected no increase in cytotoxicity when autologous lymphocytes were incubated with RNA from animals immunized either with melanoma tissue or normal skin tissue from the autochthonous host. By contrast, when allogeneic lymphocytes were used as effector cells, RNA extracted from animals immunized either with melanoma tissue or normal skin mediated cytotoxic immune reactions against melanoma target cells and normal fibroblast target cells derived from the same patient.

Antigens, Neoplasm↗
PubMed2024

Soluble immune checkpoint factors reflect exhaustion of antitumor immunity and response to PD-1 blockade.

BACKGROUNDPrecise stratification of patients with non-small cell lung cancer (NSCLC) is needed for appropriate application of PD-1/PD-L1 blockade therapy.METHODSWe measured soluble forms of the immune-checkpoint molecules PD-L1, PD-1, and CTLA-4 in plasma of patients with advanced NSCLC before PD-1/PD-L1 blockade. A prospective biomarker-finding trial (cohort A) included 50 previously treated patients who received nivolumab. A retrospective observational study was performed for patients treated with any PD-1/PD-L1 blockade therapy (cohorts B and C), cytotoxic chemotherapy (cohort D), or targeted therapy (cohort E). Plasma samples from all patients were assayed for soluble immune-checkpoint molecules with a highly sensitive chemiluminescence-based assay.RESULTSNonresponsiveness to PD-1/PD-L1 blockade therapy was associated with higher concentrations of these soluble immune factors among patients with immune-reactive (hot) tumors. Such an association was not apparent for patients treated with cytotoxic chemotherapy or targeted therapy. Integrative analysis of tumor size, PD-L1 expression in tumor tissue (tPD-L1), and gene expression in tumor tissue and peripheral CD8+ T cells revealed that high concentrations of the 3 soluble immune factors were associated with hyper or terminal exhaustion of antitumor immunity. The combination of soluble PD-L1 (sPD-L1) and sCTLA-4 efficiently discriminated responsiveness to PD-1/PD-L1 blockade among patients with immune-reactive tumors.CONCLUSIONCombinations of soluble immune factors might be able to identify patients unlikely to respond to PD-1/PD-L1 blockade as a result of terminal exhaustion of antitumor immunity. Our data suggest that such a combination better predicts, along with tPD-L1, for the response of patients with NSCLC.TRIAL REGISTRATIONUMIN000019674.FUNDINGThis study was funded by Ono Pharmaceutical Co. Ltd. and Sysmex Corporation.

Humans↗
PubMed1975

Immune mechanisms in leukemia: suppression of cellular immunity by starvation.

The effects of starvation on the cellular immune response of C58/Wm mice to syngeneic malignant lymphoid cells (1b cells) were studied. Mice were starved 1-3 days before or after immunization. The capacity of starved animals to survive immunization was used to quantify immunosuppression. When starvation bracketed immunization by -1 to +1 days, only 2 of 23 mice survived primary immunization, compared with 100% survival for nonstarved controls. A 2-day period of starvation +1 to +7 days after primary immunization reduced survival about 30%. For a test of the effect of starvation on the secondary immune response, mice were immunized, starved 2 days, and then challenged with viable lb cells. When mice were starved from -3 to +1 days before or after challenge, there was a 25-45% decrease in survival. Starvation caused a disproportionate depletion of lymphoid tissue elements. The proportional loss in the weight of the spleen and thymus was essentially twice as great as the loss in total body weight. The peripheral blood leukocyte count was reduced by about 20% when mice were starved 1 day and by approximately 50% when they were starved 2 days. When mice were starved 1-2 days, the differential leukocyte count did not shift and there was no significant change in the number of blood erythrocytes or in the hematocrit. Starvation for 2 days caused a 65-70% reduction in the number of viable mononuclear spleen cells. Starvation for 3 days caused about 90% reduction. Adoptive cell transfer experiments showed that the immunocompetence of individual spleen immunocytes was not reduced by starvation.

Animals↗
PubMed1979

Local cholera immunity in mice: intestinal antitoxin-containing cells and their correlation with protective immunity.

Methods for light and electron microscopic identification and characterization of intestinal cholera antitoxin-containing cells (ACC) using peroxidase-labeled immunoreagent are described and used to study the ACC response in mice after immunizations with cholera toxin. Specific ACC appeared in significant numbers after two oral immunizations and increased six- to eightfold with two additional oral boosters, whereas further oral immunizations caused no additional stimulation. Intravenous immunizations had to be repeated seven times before ACC could be detected. After two oral immunizations, most of the ACC were found in the proximal part of the small intestine and no ACC were seen in the colon. This uneven distribution of ACC within the small intestine was eliminated after four oral immunizations, when ACC could also be detected in the colon. The ACC response after four oral immunizations demonstrated a peak at 4 days with far fewer cells present at 2 and 7 days. Electron microscopic studies showed that the ACC were mature plasma cells with the staining localized to the endoplasmic reticulum. Regression analysis of the relationship between the number of ACC and the magnitude of protective immunity against intestinal challenge with cholera toxin indicates a highly significant correlation (r = 0.91, P less than 0.001).

Animals↗
PubMed1976

Immune processes in the course of infection with dysentery bacilli. I. Transfer of immunity by means of spleen cells.

Studies on the mechanisms of immune phenomena in the course of infections with dysentery bacilli in mice showed that injection of live Shigella sonnei phase I bacilli intravenously evokes the appearance in the spleen of cells by means of which immunity to a lethal dose of these microorganisms can be transferred into other mice. Immunity to a lethal dose of the bacteria was measured by the number of animals surviving the infection, and by the numbers of bacteria isolated from the organs of the animals. "Active" cells appeared in the spleen 4-8 days after immunization. Spleen cells obtained from mice earlier than 4-8 days after immunization, or from non-immunized mice, were inactive. The role of cell-mediated immunity, reactivity to endotoxins per se, and specific immunoglobulins in immunity to bacterial dysentery in mice are discussed.

Animals↗
PubMed2025

Tumor-immune partitioning and clustering algorithm for identifying tumor-immune cell spatial interaction signatures within the tumor microenvironment.

BACKGROUND: Growing evidence supports the importance of characterizing the organizational patterns of various cellular constituents in the tumor microenvironment in precision oncology. Most existing data on immune cell infiltrates in tumors, which are based on immune cell counts or nearest neighbor-type analyses, have failed to fully capture the cellular organization and heterogeneity. METHODS: We introduce a computational algorithm, termed Tumor-Immune Partitioning and Clustering (TIPC), that jointly measures immune cell partitioning between tumor epithelial and stromal areas and immune cell clustering versus dispersion. As proof-of-principle, we applied TIPC to a prospective cohort incident tumor biobank containing 931 colorectal carcinoma cases. TIPC identified tumor subtypes with unique spatial patterns between tumor cells and T lymphocytes linked to certain molecular pathologic and prognostic features. T lymphocyte identification and phenotyping were achieved using multiplexed (multispectral) immunofluorescence. In a separate hepatocellular carcinoma cohort, we replaced the stromal component with specific immune cell types-CXCR3+CD68+ or CD8+-to profile their spatial relationships with CXCL9+CD68+ cells. RESULTS: Six unsupervised TIPC subtypes based on T lymphocyte distribution patterns were identified, comprising two cold and four hot subtypes. Three of the four hot subtypes were associated with significantly longer colorectal cancer (CRC)-specific survival compared to a reference cold subtype. Our analysis showed that variations in T-cell densities among the TIPC subtypes did not strictly correlate with prognostic benefits, underscoring the prognostic significance of immune cell spatial patterns. Additionally, TIPC revealed two spatially distinct and cell density-specific subtypes among microsatellite instability-high colorectal cancers, indicating its potential to upgrade tumor subtyping. TIPC was also applied to additional immune cell types, eosinophils and neutrophils, identified using morphology and supervised machine learning; here two tumor subtypes with similarly low densities, namely 'cold, tumor-rich' and 'cold, stroma-rich', exhibited differential prognostic associations. Lastly, we validated our methods and results using The Cancer Genome Atlas colon and rectal adenocarcinoma data (n = 570). Moreover, applying TIPC to hepatocellular carcinoma cases (n = 27) highlighted critical cell interactions like CXCL9-CXCR3 and CXCL9-CD8. CONCLUSIONS: Unsupervised discoveries of microgeometric tissue organizational patterns and novel tumor subtypes using the TIPC algorithm can deepen our understanding of the tumor immune microenvironment and likely inform precision cancer immunotherapy.

Humans↗
PubMedDate not supplied

Studies on Pasteurella multocida. VI. Nature of systemic immunity and analysis of the correlation between levels of immunity induced by various fowl cholera vaccines and protection against challenge.

The nature of the systemic immunity induced by various vaccines against fowl cholera disease in turkeys was investigated. Used as vaccines were three avirulent strains (CU, M2283, and P1580) of Pasteurella multocida administered in the drinking water and a bacterin administered parenterally. A passive hemagglutination test was developed to measure levels of systemic humoral immunity. Systemic cell-mediated immune response was assayed by an in vitro immunostimulation microculture system utilizing peripheral blood lymphocytes. The bacterin induced high levels of systemic humoral and cell-mediated immune responses which respectively persisted for 8 and 6 weeks. The CU strain of live vaccine induced average levels of systemic immunity (humoral and cell-mediated) which respectively persisted for 4 and 6 weeks. The M2283 strain of live vaccine also induced average levels of systemic immunity (less than induced by the CU strain) which respectively persisted for 4 and 6 weeks. The P1580 strain of live vaccine induced low levels of systemic immunity which persisted for only 2 weeks. Results from data generated from an analysis of correlation between levels of immunity and protection indicate that systemic immunity (humoral and cell-mediated) played a significant role.

Administration, Oral↗
PubMed1978

Immunological characteristics of leukemia and lymphoma in allogeneic cell immunity: growth of syngeneic tumors in rats immunized with allogeneic cells.

The growth of transplanted tumors was strongly inhibited in syngeneic Wistar King Aptekman (WKA) rats immunized with allogeneic tumor cells from Donryu rats. This phenomenon of non-specific immunity against tumors is referred to as "allogeneic cell immunity". However, an exception to the "allogeneic cell immunity" was observed in leukemias and lymphomas. Four transplanted leukemia or lymphoma lines were not inhibited in syngeneic rats immunized with allogenic tumor cells. Furthermore, immunization with allogeneic leukemic cells had only a relatively weak inhibitory effect upon a syngeneic fibrosarcoma and no inhibitory effect upon leukemias. In WKA rats immunized with allogeneic lymphoid cells from Donryu rats, the growth of fibrosarcoma, but not of lymphoma, was inhibited. Using transplantation experiments, both fibrosarcoma and lymphoma were defined as antigenic tumors in WKA rats. Transplantation of mixtures of syngeneic tumor cells and allogeneic tumor cells in WKA rats confirmed the above findings. These results revealed that leukemia and lymphoma differ from non-leukemic tumors in regard to "allogeneic cell immunity".

Animals↗
PubMed2026

HLA class I expression and tumor immune infiltration together shape colon cancer immune contexture.

BACKGROUND: The relative contribution of HLA class I molecules-including classical HLA class Ia (HLA-A, -B, -C) and non-classical HLA class Ib (HLA-E, -F, -G)-to shaping the tumor immune microenvironment in colon cancer remains insufficiently defined. We investigated how their expression patterns relate to immune infiltration and clinical outcome. METHODS: In a retrospective cohort of 280 colon cancers, we assessed HLA class Ia and class Ib expression and quantified CD45-positive immune cell infiltration by immunohistochemistry. These features were correlated with clinicopathological variables, microsatellite instability (MSI) status, and previously established genomic immune signatures. RESULTS: High HLA class Ia expression and increased CD45-positive cell infiltration were each associated with improved overall, disease-specific, and progression-free survival. CD45-positive density correlated strongly with Immunologic Constant of Rejection scores. HLA class Ia loss was more frequent in advanced stages and in MSI-H tumors. Among HLA class Ib molecules, only HLA-E expression was associated with favorable disease-specific and progression-free survival. Integrative analysis identified three immune phenotypes with distinct prognostic profiles; tumors characterized by high HLA class Ia expression, low HLA class Ib expression, and high CD45-positive infiltration had the best outcomes. CONCLUSION: Colon cancer immunogenicity is shaped by coordinated patterns of HLA class I expression and immune infiltration. Integrating HLA class Ia/Ib expression with immune cell density provides a refined stratification of tumor immune phenotypes and may support personalized immunotherapeutic decision-making.

Antigen presentation↗
PubMed1977

Inability of spleen cells from chancre-immune rabbits to confer immunity to challenge with Treponema pallidum.

Although several lines of evidence suggest that cellular immune mechanisms play a role in controlling infection due to Treponema pallidum, recent studies have shown that induction of acquired cellular resistance by antigenically unrelated organisms fails to protect rabbits against syphilitic infection, thereby casting doubt on this hypothesis. In the present paper we describe attempts to transfer immunity to syphilis by using spleen cells from chancre-immune rabbits. Intravenous infusion of 2 X 10(8) spleen lymphocytes was capable of transferring acquired cellular resistance to Listeria and delayed hypersensitivity to tuberculin. However, in eight separate experiments using outbred or inbred rabbits, 2 X 10(8) spleen cells from syphilis-immune animals failed to confer resistance to T. pallidum whether by intravenous or intradermal challenge. Mixing immune lymphocytes with treponemes immediately before intradermal inoculation also failed to confer resistance. Despite the fact that syphilitic infection stimulates cellular immune mechanisms and induces acquired cellular resistance to antigenically unrelated organisms, cellular immunity may not play an important role in immunity to syphilis.

Animals↗
PubMed1977

Expermental glomerulonephritis in the rat induced by antibodies directed against tubular antigens. III. In vitro evaluation of cell-mediated immune responses against immune complexes influenced by immunosuppressive therapy.

In this paper, cell-mediated immunity (CMI) as evaluated by in vitro migration inhibition assays an in vivo delayed type skin reactions in experimental immune complex glomerulonephritis (ECGN) was studied as well as the effect of treatment with immunosuppressive drugs on these immune responses. In glomerulonephritic rats MIF production as well as delayed type skin reactions could be demonstrated directed against tubular brushborder antigen (Fx1A) containing immune complexes or to their constituents (FX1A or rabbit IgG). Treatment of the animals with immunosuppressive drugs during settled disease state (autologous phase) abolished these cellular immune reactions. However, neither the glomerular depositions of rat IgG associated with the autologous phase, nor the urinary excretion was influenced. When treatment of the animals was started simultaneously with the induction of the ECGN both cellular and humoral immune responses as well as proteinuria were affected. It was concluded that although in this glomerulonephritis model specific MIF response after specific stimulation in vitro as well as DTH reactions could be detected against immune complexes or their constituents, these immune reactions seem not to play important role in this ECGN in particular with respect to the proteinuria.

Animals↗
PubMedDate not supplied

[Relationship between orally induced immune tolerance and local immune response (author's transl)].

BALB/c mice were immunized by intragastric immunization with sheep red blood cells repeated daily for 4 days. This immunization resulted in the appearance of circulating antibodies which were predominantly of the IgA class. When serum from intragastrically immunized mice was administered intraperitoneally to recipient animals 8 h before parenteral immunization with sheep red blood cells, the subsequent immune response was depressed proportionally to the dose of serum injected. When intragastrically immunized mice were challenged intraperitoneally with sheep red blood cells, the level of the IgM response to the parenteral stimulation was in inverse ratio to the IgA response induced by the oral route. These results suggest that orally induced IgA production is related to orally induced immune tolerance and that systemic hyporesponsiveness is achieved while gut plasma cells are producing specific IgA.

Administration, Oral↗