In vivo and in vitro cell-mediated immunity to tetanus toxoid in adults

ABSTRACT The 70-kDa recombinant Candida albicans heat shock protein (CaHsp70) and its 21-kDa C-terminal and 28-kDa N-terminal fragments (CaHsp70-Cter and CaHsp70-Nter, respectively) were studied for their immunogenicity, including proinflammatory cytokine induction in vitro and in vivo, and protection in a murine model of hematogenous candidiasis. The whole protein and its two fragments were strong inducers of both antibody (Ab; immunoglobulin G1 [IgG1] and IgG2b were the prevalent isotypes) and cell-mediated immunity (CMI) responses in mice. CaHsp70 preparations were also recognized as CMI targets by peripheral blood mononuclear cells of healthy human subjects. Inoculation of CaHsp70 preparations into immunized mice induced rapid production of interleukin-6 (IL-6) and tumor necrosis factor alpha, peaking at 2 to 5 h and declining within 24 h. CaHsp70 and CaHsp70-Cter also induced gamma interferon (IFN-γ), IL-12, and IL-10 but not IL-4 production by CD4+ lymphocytes cocultured with splenic accessory cells from nonimmunized mice. In particular, the production of IFN-γ was equal if not superior to that induced in the same cells by whole, heat-inactivated fungal cells or the mitogenic lectin concanavalin A. In immunized mice, however, IL-4 but not IL-12 was produced in addition to IFN-γ upon in vitro stimulation of CD4+ cells with CaHsp70 and CaHsp70-Cter. These animals showed a decreased median survival time compared to nonimmunized mice, and their mortality was strictly associated with organ invasion by fungal hyphae. Their enhanced susceptibility was attributable to the immunization state, as it did not occur in congenitally athymic nude mice, which were unable to raise either Ab or CMI responses to CaHsp70 preparations. Together, our data demonstrate the elevated immunogenicity of CaHsp70, with which, however, no protection against but rather some enhancement of Candida infection seemed to occur in the mouse model used.

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Immunity to pathogenic free-living amoebae: role of cell-mediated immunity

Infection and Immunity ◽

10.1128/iai.29.2.408-410.1980 ◽

1980 ◽

Vol 29 (2) ◽

pp. 408-410

Author(s):

R T Cursons ◽

T J Brown ◽

E A Keys ◽

K M Moriarty ◽

D Till

Keyword(s):

Immune System ◽

Inhibition Test ◽

Delayed Hypersensitivity ◽

Cell Mediated Immunity ◽

Pathogenic Species ◽

Free Living

The role of cell-mediated immunity in defense against pathogenic free-living amoebae was examined. Both the in vitro macrophage inhibition test and the in vivo delayed hypersensitivity test showed responses to both heterologous and homologous antigens, although homologous systems were the most efficient. It is suggested that exposure to nonpathogenic species of free-living amoebae can stimulate the immune system to be effective against pathogenic species. The significance of cell-mediated immunity as a defense against invasion by pathogenic free-living amoebae is discussed.

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Development of suppressor T lymphocytes for Epstein-Barr virus-induced B-lymphocyte outgrowth during acute infectious mononucleosis: assessment by two quantitative systems

Blood ◽

10.1182/blood.v57.3.510.510 ◽

1981 ◽

Vol 57 (3) ◽

pp. 510-517 ◽

Cited By ~ 20

Author(s):

RT Schooley ◽

BF Haynes ◽

J Grouse ◽

C Payling-Wright ◽

AS Fauci ◽

...

Keyword(s):

T Lymphocytes ◽

B Lymphocytes ◽

Epstein Barr Virus ◽

B Lymphocyte ◽

Acute Stage ◽

Cell Mediated Immunity ◽

Barr Virus ◽

Epstein Barr

Abstract A system of 3H-thymidine incorporation by lymphocytes in culture for 3 wk has been utilized for quantitative assessment of the ability of T lymphocytes to inhibit outgrowth of autologous Epstein-Barr virus (EBV) transformed B lymphocytes. Lymphocytes from EBV-seronegative individuals lack the ability to suppress outgrowth of autologous EBV- transformed B lymphocytes. This capability appears during the course of primary EBV-induced infectious mononucleases (IM) as the atypical lymphocytosis is subsiding and persists for years after recovery from primary EBV infection. The ability of T lymphocytes from EBV- seropositive subjects or convalescent IM patients to inhibit B- lymphocyte outgrowth is not HLA restricted. Thus, T lymphocytes capable of inhibition of in vitro EBV-induced B-cell outgrowth emerge during the acute stage of IM and may represent an important control mechanism of EBV-induced B-lymphocyte proliferation in vivo. The system provides a highly sensitive quantitative means for in vitro assessment of cell- mediated immunity to EBV.

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The immunoregulation of mesenchymal stem cells plays a critical role in improving the prognosis of liver transplantation

Journal of Translational Medicine ◽

10.1186/s12967-019-02167-0 ◽

2019 ◽

Vol 17 (1) ◽

Cited By ~ 5

Author(s):

Chenxia Hu ◽

Lanjuan Li

Keyword(s):

Liver Transplantation ◽

Natural Killer ◽

Immune Cells ◽

Adaptive Systems ◽

Critical Role ◽

Arterial System ◽

Cell Mediated Immunity ◽

Adaptive Immune Cells

AbstractThe liver is supplied by a dual blood supply, including the portal venous system and the hepatic arterial system; thus, the liver organ is exposed to multiple gut microbial products, metabolic products, and toxins; is sensitive to extraneous pathogens; and can develop liver failure, liver cirrhosis and hepatocellular carcinoma (HCC) after short-term or long-term injury. Although liver transplantation (LT) serves as the only effective treatment for patients with end-stage liver diseases, it is not very popular because of the complications and low survival rates. Although the liver is generally termed an immune and tolerogenic organ with adaptive systems consisting of humoral immunity and cell-mediated immunity, a high rejection rate is still the main complication in patients with LT. Growing evidence has shown that mesenchymal stromal cell (MSC) transplantation could serve as an effective immunomodulatory strategy to induce tolerance in various immune-related disorders. MSCs are reported to inhibit the immune response from innate immune cells, including macrophages, dendritic cells (DCs), natural killer cells (NK cells), and natural killer T (NKT) cells, and that from adaptive immune cells, including T cells, B cells and other liver-specific immune cells, for the generation of a tolerogenic microenvironment. In this review, we summarized the relationship between LT and immunoregulation, and we focused on how to improve the effects of MSC transplantation to improve the prognosis of LT. Only after exhaustive clarification of the potential immunoregulatory mechanisms of MSCs in vitro and in vivo can we implement MSC protocols in routine clinical practice to improve LT outcome.

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In VitroImmune Competence of Buffaloes (Bubalus bubalis) of Different Production Potential: Effect of Heat Stress and Cortisol

Veterinary Medicine International ◽

10.4061/2011/860252 ◽

2011 ◽

Vol 2011 ◽

pp. 1-5 ◽

Cited By ~ 2

Author(s):

Joydip Mukherjee ◽

Sujata Pandita ◽

Ruokuobeinuo Huozha ◽

Manju Ashutosh

Keyword(s):

Heat Stress ◽

Stimulation Index ◽

Bubalus Bubalis ◽

Potential Effect ◽

Production Level ◽

Cell Mediated Immunity ◽

Lymphocyte Proliferation Response ◽

Proliferation Response

Twelve healthy lactating Murrah buffaloes of similar parity (3rd) between 90 and 120 days of lactation, selected from the herd of National Dairy Research Institute (Karnal, India) and maintained at managemental practices as followed at the Institute they were included in this experiment. The animals were divided into two groups based on their production level in previous lactation. The average milk production level of group 1 and II was 9.3 and 6 lit/day, respectively. Blood was collected from these buffaloes on three occasions 10 days apart. The lymphocytes were separated and cultured in RPMI 1640 medium with PHA-P for 24 h at 37°C in a humidified CO2incubator (95% air and 5% CO2). The lymphocyte responsiveness was also evaluated in response to thein vivoheat stress andin vitrocortisol. Mitogen-induced stimulation index was not affected by production level (). Stimulation index was significantly reduced () in both the groups when cortisol was added at 2.0 ng level in the culture. However, in heat-stressed buffaloes stimulation index did not vary despite increasing levels of cortisol, thus indicating that lymphocyte may become cortisol resistant during periods of acute heat stress. The results showed that lymphocyte proliferation response can be effectively used to study buffalo cell-mediated immunityin vitro.

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Migration ofAntigen-Specific T Cells Away from CXCR4-Binding Human ImmunodeficiencyVirus Type 1gp120

Journal of Virology ◽

10.1128/jvi.78.10.5184-5193.2004 ◽

2004 ◽

Vol 78 (10) ◽

pp. 5184-5193 ◽

Cited By ~ 18

Author(s):

Diana M. Brainard ◽

William G. Tharp ◽

Elva Granado ◽

Nicholas Miller ◽

Alicja K. Trocha ◽

...

Keyword(s):

T Cells ◽

T Cell ◽

Immune Cell ◽

Active Movement ◽

Target Cells ◽

Cell Mediated Immunity ◽

Cell Trafficking ◽

Hiv 1

ABSTRACT Cell-mediated immunity depends in part on appropriate migration and localization of cytotoxic T lymphocytes (CTL), a process regulated by chemokines and adhesion molecules. Many viruses, including human immunodeficiency virus type 1 (HIV-1), encode chemotactically active proteins, suggesting that dysregulation of immune cell trafficking may be a strategy for immune evasion. HIV-1 gp120, a retroviral envelope protein, has been shown to act as a T-cell chemoattractant via binding to the chemokine receptor and HIV-1 coreceptor CXCR4. We have previously shown that T cells move away from the chemokine stromal cell-derived factor 1 (SDF-1) in a concentration-dependent and CXCR4 receptor-mediated manner. Here, we demonstrate that CXCR4-binding HIV-1 X4 gp120 causes the movement of T cells, including HIV-specific CTL, away from high concentrations of the viral protein. This migratory response is CD4 independent and inhibited by anti-CXCR4 antibodies and pertussis toxin. Additionally, the expression of X4 gp120 by target cells reduces CTL efficacy in an in vitro system designed to account for the effect of cell migration on the ability of CTL to kill their target cells. Recombinant X4 gp120 also significantly reduced antigen-specific T-cell infiltration at a site of antigen challenge in vivo. The repellant activity of HIV-1 gp120 on immune cells in vitro and in vivo was shown to be dependent on the V2 and V3 loops of HIV-1 gp120. These data suggest that the active movement of T cells away from CXCR4-binding HIV-1 gp120, which we previously termed fugetaxis, may provide a novel mechanism by which HIV-1 evades challenge by immune effector cells in vivo.

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Impaired In Vivo Immune Responses in Patients with Melancholia

The British Journal of Psychiatry ◽

10.1192/bjp.162.5.651 ◽

1993 ◽

Vol 162 (5) ◽

pp. 651-657 ◽

Cited By ~ 61

Author(s):

Ian Hickie ◽

Catherine Hickie ◽

Andrew Lloyd ◽

Derrick Silove ◽

Denis Wakefield

Keyword(s):

Immune Responses ◽

Delayed Type Hypersensitivity ◽

Cell Mediated Immunity ◽

Melancholic Depression ◽

Skin Responses ◽

Severity Of Depression ◽

Depressive Subtypes ◽

Control Study

Previous attempts to establish a relationship between impaired cell-mediated immunity (CMI) and major mood disorders have been limited by a failure to explore the relevance of depressive subcategories or to assess CMI by in vivo methods. In this case-control study CMI was assessed in 57 patients with major depression (31 with melancholic, 26 with non-melancholic disorders), and in age- and sex-matched controls by both in vitro and in vivo immunological techniques. Compared with control subjects and patients with non-melancholic depression, patients with melancholia demonstrated reduced in vivo CMI as assessed by delayed-type hypersensitivity (DTH) skin responses. Although increasing age, severity of depression, hospital admission for treatment, and reported weight loss are correlates of melancholia, none of these factors alone, or in combination, accounted for the differences in DTH responses observed between the two depressive subtypes. These data suggest that impaired CMI in vivo may be limited to those with melancholic disorders. At this stage the factors which account for this effect are unclear.

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Binding of HMG-I(Y) Imparts Architectural Specificity to a Positioned Nucleosome on the Promoter of the Human Interleukin-2 Receptor α Gene

Molecular and Cellular Biology ◽

10.1128/mcb.20.13.4666-4679.2000 ◽

2000 ◽

Vol 20 (13) ◽

pp. 4666-4679 ◽

Cited By ~ 42

Author(s):

R. Reeves ◽

W. J. Leonard ◽

M. S. Nissen

Keyword(s):

T Cell ◽

Transcriptional Activation ◽

Interleukin 2 ◽

Proximal Promoter ◽

Cell Mediated Immunity ◽

Core Particle ◽

The Core ◽

Interleukin 2 Receptor

ABSTRACT Transcriptional induction of the interleukin-2 receptor alpha-chain (IL-2Rα) gene is a key event regulating T-cell-mediated immunity in mammals. In vivo, the T-cell-restricted protein Elf-1 and the general architectural transcription factor HMG-I(Y) cooperate in transcriptional regulation of the human IL-2Rα gene by binding to a specific positive regulatory region (PRRII) in its proximal promoter. Employing chromatin reconstitution analyses, we demonstrate that the binding sites for both HMG-I(Y) and Elf-1 in the PRRII element are incorporated into a strongly positioned nucleosome in vitro. A variety of analytical techniques was used to determine that a stable core particle is positioned over most of the PRRII element and that this nucleosome exhibits only a limited amount of lateral translational mobility. Regardless of its translational setting, the in vitro position of the nucleosome is such that DNA recognition sequences for both HMG-I(Y) and Elf-1 are located on the surface of the core particle. Restriction nuclease accessibility analyses indicate that a similarly positioned nucleosome also exists on the PRRII element in unstimulated lymphocytes when the IL-2Rα gene is silent and suggest that this core particle is remodeled following transcriptional activation of the gene in vivo. In vitro experiments employing the chemical cleavage reagent 1,10-phenanthroline copper (II) covalently attached to its C-terminal end demonstrate that HMG-I(Y) protein binds to the positioned PRRII nucleosome in a direction-specific manner, thus imparting a distinct architectural configuration to the core particle. Together, these findings suggest a role for the HMG-I(Y) protein in assisting the remodeling of a critically positioned nucleosome on the PRRII promoter element during IL-2Rα transcriptional activation in lymphocytes in vivo.

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