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  1. Article: Respiratory tract cell-mediated immunity: comparison of primary and secondary response.

    Gadol, N / Johnson, J E / Waldman, R H

    Infection and immunity

    1974  Volume 9, Issue 5, Page(s) 858–862

    Abstract: A secondary local and splenic cell-mediated immune response was observed and compared ... This study evaluated the secondary as compared to the primary response, with respect to both cellular and ... to the primary response. Previous studies have demonstrated cell-mediated immunity (CMI) by lymphocytes ...

    Abstract A secondary local and splenic cell-mediated immune response was observed and compared to the primary response. Previous studies have demonstrated cell-mediated immunity (CMI) by lymphocytes from bronchopulmonary washings and have shown that its appearance is to a large extent inedpendent of splenic CMI. This study evaluated the secondary as compared to the primary response, with respect to both cellular and humoral immune responses. Guinea pigs were immunized with influenza virus vaccine either nasally or parenterally, booster immunizations were given by the same route, and animals were killed at various times after immunization or booster. The inhibition of macrophage migration was used to assess CMI. As in previous studies, local application of antigen led to mainly local appearance of CMI, whereas parenteral immunization led to mainly systemic CMI. Both pulmonary and splenic lymphocytes showed an inhibition of macrophage migration that appeared 2 to 3 days sooner after the booster, as compared to the primary immunization. There was no evidence, however, for the earlier production or increased amount of antibody in the bronchial secretions in the boosted animals. The results suggest that pulmonary as well as splenic T lymphocytes exhibit memory, but that pulmonary B lymphocytes do not.
    MeSH term(s) Animals ; Antibodies, Viral/analysis ; Cell Migration Inhibition ; Guinea Pigs ; Hemadsorption ; Immunity, Cellular ; Immunization ; Immunization, Secondary ; Immunologic Memory ; Influenza Vaccines ; Lung/cytology ; Macrophages/immunology ; Neutralization Tests ; Respiratory System/immunology ; Respiratory Tract Infections/immunology ; Spleen/cytology
    Chemical Substances Antibodies, Viral ; Influenza Vaccines
    Language English
    Publishing date 1974-05
    Publishing country United States
    Document type Comparative Study ; Journal Article
    ZDB-ID 218698-6
    ISSN 1098-5522 ; 0019-9567
    ISSN (online) 1098-5522
    ISSN 0019-9567
    DOI 10.1128/iai.9.5.858-862.1974
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 684: Show issues Location:
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  2. Article ; Online: STAT4 deficiency fails to induce lung Th2 or Th17 immunity following primary or secondary respiratory syncytial virus (RSV) challenge but enhances the lung RSV-specific CD8+ T cell immune response to secondary challenge.

    Dulek, Daniel E / Newcomb, Dawn C / Toki, Shinji / Goliniewska, Kasia / Cephus, Jacqueline / Reiss, Sara / Bates, John T / Crowe, James E / Boyd, Kelli L / Moore, Martin L / Zhou, Weisong / Peebles, R Stokes

    Journal of virology

    2014  Volume 88, Issue 17, Page(s) 9655–9672

    Abstract: ... adaptive immune responses to viral infection. Our results show that STAT4 regulates the immune response to primary and ... We performed primary and secondary RSV challenges in WT and STAT4-/- mice and used STAT1-/- mice as a positive ... primary and secondary RSV infections. ...

    Abstract Unlabelled: Immune-mediated lung injury is a hallmark of lower respiratory tract illness caused by respiratory syncytial virus (RSV). STAT4 plays a critical role in CD4+ Th1 lineage differentiation and gamma interferon (IFN-γ) protein expression by CD4+ T cells. As CD4+ Th1 differentiation is associated with negative regulation of CD4+ Th2 and Th17 differentiation, we hypothesized that RSV infection of STAT4-/- mice would result in enhanced lung Th2 and Th17 inflammation and impaired lung Th1 inflammation compared to wild-type (WT) mice. We performed primary and secondary RSV challenges in WT and STAT4-/- mice and used STAT1-/- mice as a positive control for the development of RSV-specific lung Th2 and Th17 inflammation during primary challenge. Primary RSV challenge of STAT4-/- mice resulted in decreased T-bet and IFN-γ expression levels in CD4+ T cells compared to those of WT mice. Lung Th2 and Th17 inflammation did not develop in primary RSV-challenged STAT4-/- mice. Decreased IFN-γ expression by NK cells, CD4+ T cells, and CD8+ T cells was associated with attenuated weight loss and enhanced viral clearance with primary challenge in STAT4-/- mice compared to WT mice. Following secondary challenge, WT and STAT4-/- mice also did not develop lung Th2 or Th17 inflammation. In contrast to primary challenge, secondary RSV challenge of STAT4-/- mice resulted in enhanced weight loss, an increased lung IFN-γ expression level, and an increased lung RSV-specific CD8+ T cell response compared to those of WT mice. These data demonstrate that STAT4 regulates the RSV-specific CD8+ T cell response to secondary infection but does not independently regulate lung Th2 or Th17 immune responses to RSV challenge.
    Importance: STAT4 is a protein critical for both innate and adaptive immune responses to viral infection. Our results show that STAT4 regulates the immune response to primary and secondary challenge with RSV but does not restrain RSV-induced lung Th2 or Th17 immune responses. These findings suggest that STAT4 expression may influence lung immunity and severity of illness following primary and secondary RSV infections.
    MeSH term(s) Animals ; CD8-Positive T-Lymphocytes/immunology ; Disease Models, Animal ; Female ; Lung/immunology ; Lung/pathology ; Mice, Inbred BALB C ; Mice, Knockout ; Respiratory Syncytial Virus Infections/immunology ; Respiratory Syncytial Viruses/immunology ; STAT4 Transcription Factor/deficiency ; STAT4 Transcription Factor/immunology ; Th17 Cells/immunology ; Th2 Cells/immunology
    Chemical Substances STAT4 Transcription Factor ; Stat4 protein, mouse
    Language English
    Publishing date 2014-06-11
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 80174-4
    ISSN 1098-5514 ; 0022-538X
    ISSN (online) 1098-5514
    ISSN 0022-538X
    DOI 10.1128/JVI.03299-13
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Experimental production of granulomatous pneumonitis. Comparison of immunological and morphological sequelae with particulate and soluble antigens administered via the respiratory route.

    Salvaggio, J / Phanuphak, P / Stanford, R / Bice, D / Claman, H

    The Journal of allergy and clinical immunology

    1975  Volume 56, Issue 5, Page(s) 364–380

    Abstract: ... antigens via the respiratory route can lead to systemic humoral and cell-mediated immunity ... morphologic changes and the humoral plus cellular immunologic response. Primary respiratory tract ... developed only after secondary BSA aerosol challenge. In contrast to these findings, "primary ...

    Abstract Rabbits were sensitized with either a soluble protein antigen (BSA) or a particulate thermophilic actinomycete antigen (Micropolyspora faeni) via the respiratory route, followed by monitoring of sequential morphologic changes and the humoral plus cellular immunologic response. Primary respiratory tract sensitization with BSA resulted in a humoral anti-BSA response, Arthus and delayed skin reactivity, and in some cases specific antigen-induced alveolar macrophage migration inhibition, all in the absence of pulmonary lesions. Lesions characterized by mild multifocal perivascular mononuclear cell infiltrates in the lungs developed only after secondary BSA aerosol challenge. In contrast to these findings, "primary" respiratory tract sensitization with M. faeni particulate antigen in saline solution resulted in the gradual development of extensive and progressive pulmonary interstitial and alveolar mononuclear cell infiltrates. These lesions were uniformly associated with specific serum precipitating antibody and delayed skin reactivity. Alveolar macrophage migration was significantly inhibited by Micropolyspora faeni in virtually of these animals. These results, while not excluding a primary irritant effect or Type II or III alergic tissue injury, suggest a role for delayed (cell-mediated) hypersensitivity in the pathogenesis of particulate actinomycete-induced pulmonary lesions. They also indicate that primary immunization with soluble purified protein antigens via the respiratory route can lead to systemic humoral and cell-mediated immunity without production of pulmonary lesions.
    MeSH term(s) Actinomycetaceae/immunology ; Aerosols ; Animals ; Antibodies, Bacterial/analysis ; Antibody Formation/drug effects ; Antigens, Bacterial/administration & dosage ; Antigens, Bacterial/isolation & purification ; Cell Migration Inhibition ; Fluorescent Antibody Technique ; Granulocytes/immunology ; Histiocytes/immunology ; Injections ; Lymphocytes/immunology ; Macrophage Migration-Inhibitory Factors/analysis ; Macrophages/immunology ; Pneumonia/immunology ; Pneumonia/pathology ; Rabbits ; Respiratory Hypersensitivity/immunology ; Serum Albumin, Bovine/immunology ; Skin Tests ; Trachea
    Chemical Substances Aerosols ; Antibodies, Bacterial ; Antigens, Bacterial ; Macrophage Migration-Inhibitory Factors ; Serum Albumin, Bovine (27432CM55Q)
    Language English
    Publishing date 1975-11
    Publishing country United States
    Document type Comparative Study ; Journal Article ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 121011-7
    ISSN 1085-8725 ; 1097-6825 ; 0091-6749
    ISSN (online) 1085-8725 ; 1097-6825
    ISSN 0091-6749
    DOI 10.1016/0091-6749(75)90130-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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