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Query: UMLS:C0153470 (Spleen)
 4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The development of a cell-mediated immune response to Sendai virus infection in mice was examined by the use of a 51Cr release assay of cytotoxicity. A low level of "background cytotoxicity" to Sendai virus-infected L cells was found in the spleens of uninfected CBA mice. Spleen cells from Sendai-infected mice showed an elevated level of cytotoxicity against these target cells for a period of 5 weeks, commencing 4 days after infection of the mice. A more transient response was observed in the spleens of mice infected with a serologically distinct virus, the Kunz strain of influenza. This cross-reacting, cell-mediated immune response was intermediate between that observed in unsensitized and Sendai-sensitized spleen cells. The relevance of these cell-mediated immune responses to respiratory tract virus infections is discussed.
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PMID:Cell-mediated immunity to Sendai virus infection in mice. 18 66

The development of local and systemic cell mediated immunity (CMI) was investigated in rabbits after intratracheal immunization with live or inactivated influenza A virus. Lymphocytes from bronchoalveolar washings and draining lymph nodes were used for the assay of local CMI response. Spleen cells were employed for determination of systemic responses. Since alveolar macrophages were found to be susceptible to the action of migration inhibiting factor, the development of CMI in lungs was assayed by macrophage migration inhibition test using bronchoalveolar was cells. Immunization with live virus induces beter local CMI response than inactivated virus. After primary immunization the peak responses were found between second and third week. The secondary response was detectable much earlier and peaked at one week after booster. Small amounts of inactivates virus, which was unsufficient to evoke a primary response, could elicit a strong secondary response. The development of rapid and accentuated secondary response in the local lymphoid tissues suggests the presence of memory in the local CMI response. The results also show a good correlation to exist between primary local CMI response and the skin reactivity to the immunizing antigen. However, lack of such correlation during the secondary response leaves the skin tests less reliable in the evaluation of CMI in viral infections. Some of the functions of alveolar macrophages in the local immune reponses are also discussed.
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PMID:Immune responses to influenza virus in rabbits after local immunization. II. Local and systemic cell mediated response. 92 Nov 42

A primary cytotoxic T lymphocyte (CTL) response in vivo requires antigen presentation by cytosolic processing and can not in general be obtained by vaccination with soluble proteins. In the present work we have found that vaccination of mice with pre-processed synthetic peptides, corresponding to endogenous 9-mers produced in influenza A virus-infected cells, resulted in strong primary CTL responses. The generated CTL efficiently killed virus-infected target cells with preference for viral strains having the identical amino acid sequences to the peptides used for immunization. The optimal conditions for a primary in vivo CTL response was obtained with 100 micrograms peptide dissolved in incomplete Freund's adjuvant and injected s.c. at the base of tail. Spleen cells which had been primed 7-10 days earlier were restimulated for 5 days in vitro, using an optimal low peptide concentration (0.05 microM) and tested against virus-infected and peptide-treated target cells. The peptide-induced CTL were major histocompatibility complex class I restricted and CD8 positive.
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PMID:In vivo primary induction of virus-specific CTL by immunization with 9-mer synthetic peptides. 151 89

The influence of ISO, the antiviral drug of immunomodulating activity, on the course of experimental influenza infections and mixed, viral-bacterial infections was studied. Spleen leukocytes migration inhibition test, performed in vitro in the presence of specific antigens stimulating influence of the drug administered to the infected animals was observed.
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PMID:The influence of isoprinosine (ISO) on some cell immunity parameters in mice infected with influenza viruses and in mixed viral-bacterial infections. I. The release of the migration inhibiting factor from spleen leukocytes. 242 84

Balb/c mice were infected with influenza virus PR8 (H1N1) by the intranasal route. At various subsequent times, brain samples were examined for their content of catecholamine and indoleamine metabolites, and plasma corticosterone was measured. Virus infection was associated with a progressive loss of body and thymus weights, and an increase in plasma corticosterone. Spleen weight initially increased then decreased. There were also increases in the cerebral content of free tryptophan throughout the brain, and of MHPG, a major catabolite of norepinephrine, especially prominent in the hypothalamus. Thus influenza virus can be regarded as a stressor because, like behavioral stressors, it activates the hypothalamic-pituitary-adrenal axis, and increases cerebral concentrations of tryptophan and norepinephrine catabolites. These changes resemble those observed following administration of sheep red blood cells and Newcastle disease virus, noninfectious activators of the immune system, suggesting that noradrenergic and HPA activation are common concomitants of antigenic stimulation. The mediator of these effects may be interleukin-1 released by activated macrophages. It should be noted that animals infected with viruses can be expected to exhibit stress-like endocrine and neurochemical changes.
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PMID:Virus infection as a stressor: influenza virus elevates plasma concentrations of corticosterone, and brain concentrations of MHPG and tryptophan. 275 50

This study aimed to analyse the roles of Lyt 2+ and L3T4+ memory T-cell subpopulations in murine influenza infection. Previous work has shown that Lyt 2+ cytotoxic T-cell (Tc) clones can adoptively transfer protection. We therefore wished to see whether L3T4+ (Th) cells could also act as protective effector cells. Donors for adoptive cell transfer were thymectomized mice, depleted in vivo of either Lyt 2+ or L3T4+ T cells with monoclonal antibodies (MAb) and then infected with influenza virus (A/X31). Primed spleen cells, after removal of the B cells, were transferred into irradiated hosts infected simultaneously or persistently with a heterologous influenza virus and the effect on lung virus replication determined. Depletion of L3T4+ T cells suppressed the formation of IgG antibodies after influenza virus infection, indicating significant depletion of T-helper function. Yet Lyt 2+ class I MHC-restricted Tc cells were effectively primed in these mice, albeit to half the normal level. Adoptive transfer of the Lyt 2+ memory T cells cleared virus in a persistent infection within 6 days. Spleen cells selected for L3T4+ T cells cleared virus within 21 days of transfer in a simultaneous infection and reduced viral titres in a persistent infection, but not as effectively as L3T4+-depleted spleen cells. Although no Lyt 2+ cells were detected by fluorescence staining in Lyt 2+-depleted spleens, we could detect low levels of class I MHC-restricted influenza-specific Tc memory cells in host spleens following influenza infection. Therefore, whether the early viral clearance is solely due to L3T4+ T cells is not clear. Lyt 2+ memory T cells appear more efficient in this respect than L3T4+ memory T cells.
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PMID:Do L3T4+ T cells act as effector cells in protection against influenza virus infection. 282 Aug 68

The aim of the presented experiments was to estimate LIF production in the course of experimental infections with influenza viruses (of different degrees of adaptation), with S. aureus 209P and in the course of simultaneous viral-bacterial infections in mice. Spleen cells incubated with specific influenza antigens obtained according to Nath's method were used for the experiments as well as cells incubated with staphylococcal staphylolysine (Boehring Werke). The interdependence between LIF release and the degree of adaptation of viruses to lung tissue was observed. When influenza viruses APR-8 of high degree of adaptation to animal lung tissue were used, inconsiderable LIF production was observed in the early stage of observation. When the animals were infected with viruses A/Scotland/74 of low degree of adaptation, significant LIF production could be noticed since the 1st day of observation. Mixed, viral-bacterial infections influenced insignificantly LIF release. Its production was mainly conditioned by influenza viruses used for the infections.
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PMID:Cell phenomena in experimental viral-bacterial infections in mice. I. The release of leukocyte inhibiting factor (LIF) from mouse spleen leukocytes in the presence of specific antigens. 283 Aug 56

The levels of serum thymic activity (STA), the Thy-1.2 positivity of spleen "spontaneous" rosette-forming cells (SSRFCs) (measured in terms of Az sensitivity), as well as the blastogenic response to specific mitogens for T-lymphocytes, were studied in Balb/C mice after intranasal infection with A/PR/8/34 (HON1) influenza virus. As early as 12 hours, and more drastically, 24 hours the levels of STA were profoundly decreased after virus infection. Spleen Az sensitivity and blastogenic response of thymocytes and splenocytes to stimulation with Concanavalin A and Phytohemagglutinin, respectively, were depressed only later (day 2 or 3). These changes remain evident for about 1 week and later revert to normal values. All of the effects described are dose-dependent and appear to be virus related. Thence the PR8 virus infection initially induces a decrease of STA levels and secondly a impairment of thymus-derived immune functions.
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PMID:PR8 influenza virus infection impairs serum thymic activity levels and thymus-derived immune functions in mice. 286 45

Spleen cells from rabbits immunized with influenza virus cause inhibition of agglutination or hemolysis or both in a plaque assay test against virus-treated avian RBC.
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PMID:Plaques of hemagglutination inhibition by individual spleen cells from rabbits immunized with influenza viruses. 579 46

Normal dog plasma and serum, human, rat, and Swiss-Webster mouse plasma, phytohemagglutinin, sheep red cells, mumps and influenza vaccine, fibrinogen, and endotoxin injected before irradiation led to an increased number of endogenously derived spleen colonies in irradiated mice. Spleen weight and uptake of radioactive iron and iododeoxyuridine into such spleens were also increased. The relationship between these parameters of splenic hematopoiesis was unchanged by plasma injection suggesting that, while the number of colonies was increased, the composition of individual colonies was unchanged. This conclusion was supported by studies on plethoric mice in which splenic erythropoiesis is abolished. Increased splenic hematopoiesis was accompanied by an increase in the volume of packed red blood cells 10 days after irradiation. The total volume of plasma injected, the number of days of plasma injection preceding irradiation, and the route of administration were all important variables influencing the effect of plasma injections. Crude fractions of human albumin and gamma globulin, cortisol, C57BL (maternal) and DBA (paternal) mouse plasma, and isogeneic plasma were without effect. The ineffectiveness of isogeneic and closely related allogeneic plasma rendered unlikely the hypothesis that this effect represented the presence of homeostatic hematopoietic regulating factors in plasma. The increased hematopoiesis induced with plasma appeared to be limited to the spleen, for increased bone marrow hematopoiesis was not detected. Certain observations suggested that the effect of plasma may not be due to an antigenic or an inflammatory effect. From current observations, it was unclear whether the increased colonies induced by plasma were representative of expansion of the colony-forming cell pool or of increased efficiency of growth of the fraction surviving irradiation.
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PMID:Factors influencing hematopoietic spleen colony formation in irradiated mice. II. The effect of foreign materials. 606 3


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