The in vitro bactericidal activity of peritoneal and spleen cells from Listeria-resistant and -susceptible mouse strains

1986 ◽  
Vol 99 (1) ◽  
pp. 160-169 ◽  
Author(s):  
P.R. Wood ◽  
V. Spanidis ◽  
K. Frangos ◽  
C. Cheers
Keyword(s):  
Bactericidal Activity ◽  
Mouse Strains ◽  
Spleen Cells ◽  
Susceptible Mouse

scholarly journals Immunologic properties of bacterial lipopolysaccharide (LPS). II. The unresponsiveness of C3H/HeJ Mouse spleen cells to LPS-induced mitogenesis is dependent on the method used to extract LPS.

1975 ◽  
Vol 142 (6) ◽  
pp. 1488-1508 ◽  
Author(s):  
B J Skidmore ◽  
D C Morrison ◽  
J M Chiller ◽  
W O Weigle
Keyword(s):  
B Cells ◽  
Mouse Strain ◽  
Structural Integrity ◽  
Mitogenic Activity ◽  
Bacterial Lipopolysaccharide ◽  
Mouse Strains ◽  
Striking Difference ◽  
Spleen Cells ◽  
Destructive Effect

The C3H/HeJ mouse strain, previously shown to be a nonresponder to bacterial lipopolysaccharide (LPS)-induced mitogenesis in vitro, was demonstrated by the present studies to be competent to respond mitogenically to LPS, but only to LPS preparations obtained by selected extraction methods. These preparations appear to be confined to LPS isolated by mild extraction techniques, such as TCA or butanol. In contrast, those obtained by techniques utilizing phenol were only weakly stimulatory or completely nonstimulatory for spleen cells from the C3H/HeJ. All LPS preparations tested, on the other hand, were highly stimulatory for cells from another mouse strain, namely the C3H/St. The critical importance of the method of extraction of LPS on its mitogenic activity for C3H/HeJ cells was stressed by experiments in which LPS was prepared from Escherichia coli K235 using either of two procedures. In these experiments, phenol-extracted LPS, although mitogenic in the C3H/St, was completely nonstimulatory in the C3H/HeJ; whereas, butanol-extracted LPS was highly stimulatory in both strains of mice. This striking difference was attributed to a destructive effect of phenol on LPS, as demonstrated by the fact that treatment of butanol LPS with phenol resulted in a total loss of its mitogenic activity in the C3H/HeJ, but in only a partial loss in the C3H/St. In general, the mitogenic response observed with selected LPS preparations in the C3H/HeJ was quantitatively lower and more transient than that seen with the C3H/St, although qualitatively these responses appeared to be similar. This was evidenced by the observation that in both mouse strains LPS was a specific mitogen for B cells, a property which was also attributed in both strains to the same distinct structural region of the LPS molecule, that is lipid A. A preparation of LPS that failed to stimulate B cells from the C3H/HeJ nonetheless had the capacity to block activation of these B cells by a stimulatory preparation of LPS. These results strongly suggest that mitogenic stimulation of B cells by LPS is a function of the structural integrity of both the LPS molecule and putative B-cell receptors for LPS.

scholarly journals Isotypic and allotypic specificity of mouse rheumatoid factors.

1983 ◽  
Vol 157 (3) ◽  
pp. 1006-1019 ◽  
Author(s):  
J L Van Snick ◽  
V Stassin ◽  
B de Lestré
Keyword(s):  
Normal Mouse ◽  
Mouse Strains ◽  
Igg Subclass ◽  
Rheumatoid Factors ◽  
Spleen Cells ◽  
Polyclonal Activation ◽  
Old Mice ◽  
Reactive Antibody

The specificity of polyclonal mouse rheumatoid factors (RF) was analyzed by competition experiments with heat-aggregated mouse IgG subclasses. The RF spontaneously produced by three normal mouse strains (129/Sv, CBA/Ht, and C57Bl/6) and by two strains with autoimmune diseases (MRL/l and NZB) were found to consist of distinct non-cross-reactive antibody subpopulations each specific for one IgG subclass. The sera of the normal strains contained IgG1- and IgG2a-specific RF. The autoimmune strains produced an additional variety of RF that was specific for The autoimmune strains produced an additional variety of RF that was specific for IgG2b. Also, the RF secreted by spleen cells of various normal strains after in vitro polyclonal activation with lipopolysaccharide could be resolved into distinct subpopulations specific for IgG1 or IgG2a. These results were confirmed by the analysis of monoclonal RF derived from BALB/c, C57Bl/6, CBA/Ht, and 129/Sv mice: of 73 hybridomas with RF activity, 71 displayed a strict subclass specificity. The subclass predominantly recognized depended on the origin of the spleen cells used to generate the hybridomas. After polyclonal activation in vitro, a broad spectrum of different specificities was obtained with 16 RF specific for IgG1, 13 for IgG2a, and 4 for IgG2b. In contrast, 27 of 28 monoclonal RF derived from 129/Sv and BALB/c mice without prior polyclonal activation were specific for IgG2a, and of these 75% were allotype specific since they failed to react with IgG2a of the b allotype. These results demonstrate the importance of subclass specificity in the production of RF in vivo. With the exception of the IgG2b-specific clones, all these monoclonal RF reacted preferentially with heat-aggregated or antigen-bound IgG. Among the hybridomas generated by the fusion of in vitro polyclonally activated spleen cells of 4-wk-old mice, the frequency of clones with RF activity was at least 40 times higher than that of clones specific for mouse IgM, human IgG, ovalbumin, and hen lysozyme.

scholarly journals Incidence and severity of G6PI-induced arthritis are not increased in genetically distinct mouse strains upon aging

2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Nico Andreas ◽  
Sylvia Müller ◽  
Nicole Templin ◽  
Paul M. Jordan ◽  
Harald Schuhwerk ◽  
...  
Keyword(s):  
Immune Cell ◽  
Ex Vivo ◽  
Wild Type Mouse ◽  
Mouse Strains ◽  
Functional Difference ◽  
Susceptible Mouse ◽  
Age Related ◽  
Th Cell ◽  
Old Mice

Abstract Background The incidence of rheumatoid arthritis is correlated with age. In this study, we analyzed the association of the incidence and severity of glucose-6-phosphate isomerase (G6PI)-induced arthritis with age in two different mouse strains. Methods Young and very old mice from two different arthritis-susceptible wild-type mouse strains were analyzed after a single subcutaneous injection of G6PI s.c. The metabolism and the function of synoviocytes were analyzed in vitro, the production of bioactive lipid mediators by myeloid cells and synoviocytes was assessed in vitro and ex vivo by UPLC-MS-MS, and flow cytometry was used to verify age-related changes of immune cell composition and function. Results While the severity of arthritis was independent from age, the onset was delayed in old mice. Old mice showed common signs of immune aging like thymic atrophy associated with decreased CD4+ effector T cell numbers. Despite its decrease, the effector T helper (Th) cell compartment in old mice was reactive and functionally intact, and their Tregs exhibited unaltered suppressive capacities. In homeostasis, macrophages and synoviocytes from old mice produced higher amounts of pro-inflammatory cyclooxygenase (COX)-derived products. However, this functional difference did not remain upon challenge in vitro nor upon arthritis reactions ex vivo. Conclusion While old mice show a higher baseline of inflammatory functions, this does not result in increased reaction towards self-antigens in arthritis-susceptible mouse strains. Together, our data from two different mouse strains show that the susceptibility for G6PI-induced arthritis is not age-dependent.

scholarly journals Adenoviral Delivery of Interleukin-10 Fails To Attenuate Experimental Lyme Disease

2008 ◽  
Vol 76 (12) ◽  
pp. 5500-5507 ◽  
Author(s):  
Charles R. Brown ◽  
Annie Y.-C. Lai ◽  
Steven T. Callen ◽  
Victoria A. Blaho ◽  
Jennifer M. Hughes ◽  
...  
Keyword(s):  
Interleukin 10 ◽  
Lyme Arthritis ◽  
Mouse Strains ◽  
Susceptible Mouse ◽  
Lyme Carditis ◽  
Adenoviral Delivery ◽  
Severity Scores ◽  
C3h Mice

ABSTRACT Production of interleukin-10 (IL-10) by C57BL/6 mice following infection with Borrelia burgdorferi has been proposed as a mechanism whereby resistance to the development of experimental Lyme arthritis is maintained. In the current study, we sought to determine the role of IL-10 during infection of arthritis- and carditis-susceptible C3H mice. Infection of C3H IL-10−/− mice led to increased joint swelling and arthritis severity scores over those of wild-type C3H mice. Measurement of B. burgdorferi numbers in joints or disseminated tissues indicated a more efficient clearance of spirochetes in the absence of IL-10, similar to that reported in C57BL/6 IL-10−/− mice. However, in contrast to previous in vitro work, infection of C3H IL-10−/− mice led to decreased in vivo expression of the cytokines KC, IL-1β, IL-4, and IL-12p70 in the infected joints. Finally, adenoviral expression of IL-10 in the infected joints of C3H mice was unable to modulate the development of severe Lyme arthritis and had no effect on spirochete clearance or Borrelia-specific antibody production. Development of Lyme carditis appeared to be independent of modulation by IL-10. These results suggest that IL-10 limits the development of joint inflammation in both arthritis-resistant and -susceptible mouse strains infected with B. burgdorferi and that increased IL-10 production cannot rescue genetic susceptibility to development of pathology in this model.

scholarly journals Regulation of T-cell-mediated lympholysis by the murine major histocompatibility complex. I. Preferential in vitro responses to trinitrophenyl-modified self K- and D-coded gene products in parental and F1 hybrid mouse strains.

1979 ◽  
Vol 149 (6) ◽  
pp. 1379-1392 ◽  
Author(s):  
R B Levy ◽  
G M Shearer
Keyword(s):  
T Cell ◽  
T Cell Response ◽  
Mouse Strains ◽  
Response Patterns ◽  
Spleen Cells ◽  
F1 Hybrid ◽  
Ctl Response ◽  
Histocompatibility Complex ◽  
D Region

Spleen cells from H-2b,k,d C57Bl/10 congenic mice were sensitized in vitro to trinitrobenzenesulfonate (TNBS)-modified autologous spleen cells. Cold target competition studies at the lytic phase demonstrated three distinct patterns of cytotoxic responsiveness: (a) H-2b spleen cells generated approximately equivalent CTL responses against Kb and Db modified self products, (b) H-2d spleen cells generated preferential responses against Dd modified self products, and (c) H-2k spleen cells generated cytotoxic responses which could only be detected against Kk self products in association with TNP. F1 spleen cells were sensitized against autologous TNBS-treated cells. The results showed that, although H-2b parental cells generated approximately equivalent Kb-TNP- and Db-TNP-specific CTL, the presence of the H-2b haplotype did not result in the generation of (a) Dk-TNP CTL response by (H-2b x H-2k) spleen cells, nor (b) a Db CTL response by (H-2b x H-2a) F1 spleen cells. Additionally, (H-2d x H-2k) F1 cells failed to generate detectable Dd-TNP-specific CTL, although H-2d parental cells generated D-regional-specific CTL. The findings demonstrated that these F1 response patterns paralleled those of the H-2k and H-2a parents, i.e. weak or no D-region TNP-specific CTL were induced. Because (H-2d x H-2a) F1 responders stimulated with H-2d TNBS-treated cells did generate good Dd TNP responses, the results illustrated that the presence of responder genes was not sufficient to result in a D-region TNP CML. It is suggested that the absence of Kk alleles on the stimulating population is necessary for the generation of D-region TNP CTL in these F1's. Mechanisms which could account for these response patterns in parental F1 mice are discussed including immunodominance, suppression, T-cell response , and Ir-gene defects.

scholarly journals Regulatory T Cells as an Escape Mechanism to the Immune Response in Taenia crassiceps Infection

2021 ◽  
Vol 11 ◽  
Author(s):  
Laura Adalid-Peralta ◽  
Alexander Lopez-Roblero ◽  
Cynthia Camacho-Vázquez ◽  
Marisol Nájera-Ocampo ◽  
Adrián Guevara-Salinas ◽  
...  
Keyword(s):  
Post Infection ◽  
Proliferative Response ◽  
T Regulatory Cells ◽  
Mouse Strains ◽  
Cell Contact ◽  
Susceptible Mouse ◽  
Taenia Crassiceps ◽  
Effector Cells ◽  
Susceptibility To Infection

Murine cysticercosis by Taenia crassiceps is a model for human neurocysticercosis. Genetic and/or immune differences may underlie the higher susceptibility to infection in BALB/cAnN with respect to C57BL/6 mice. T regulatory cells (Tregs) could mediate the escape of T. crassiceps from the host immunity. This study is aimed to investigate the role of Tregs in T. crassiceps establishment in susceptible and non-susceptible mouse strains. Treg and effector cells were quantified in lymphoid organs before infection and 5, 30, 90, and 130 days post-infection. The proliferative response post-infection was characterized in vitro. The expression of regulatory and inflammatory molecules was assessed on days 5 and 30 post-infection. Depletion assays were performed to assess Treg functionality. Significantly higher Treg percentages were observed in BALB/cAnN mice, while increased percentages of activated CD127+ cells were found in C57BL/6 mice. The proliferative response was suppressed in susceptible mice, and Treg proliferation occurred only in susceptible mice. Treg-mediated suppression mechanisms may include IL-10 and TGFβ secretion, granzyme- and perforin-mediated cytolysis, metabolic disruption, and cell-to-cell contact. Tregs are functional in BALB/cAnN mice. Therefore Tregs could be allowing parasite establishment and survival in susceptible mice but could play a homeostatic role in non-susceptible strains.

scholarly journals Genetic and cellular aspects of xenogeneic mixed leukocyte culture reaction.

1976 ◽  
Vol 144 (2) ◽  
pp. 305-318 ◽  
Author(s):  
K F Lindahl ◽  
F H Bach
Keyword(s):  
T Cells ◽  
Human Lymphocytes ◽  
Mouse Strains ◽  
Target Cells ◽  
Thymidine Uptake ◽  
Spleen Cells ◽  
Proliferating Cells ◽  
Specific Antigens ◽  
Species Specific

The nature of the antigens stimulating xenogeneic lymphocytes was studied using "primed LD typing". Human lymphocytes were sensitized in vitro against mouse spleen cells and restimulated with spleen cells of mouse strains sharing non-H-2 antigens or various regions of H-2 with the initial stimulating strain. The largest thymidine uptake was caused by restimulation with cells from the specific primary stimulator or an H-2-identical strain. Species-specific antigens or strain-specific antigens carried in the C57BL/10 background account for less than 15% of the total stimulation; a non-H-2 antigen associated with the Mlsalpha genotype caused moderate restimulation, amounting to 25% of the average H-2 response. Within H-2, the strongest restimulation was caused by antigens controlled by the I-A subregion; the K and D regions caused moderate, the I-C and S regions very weak, and the I-B subregion no restimulation. Thus, the genetic control of antigens stimulating xenogeneic and allogeneic MLC responses requires T cells and adherent cells, but in the human-mouse MLC, both cell types must come from the human responder; the majority of the proliferating cells are T cells. It is suggested that allograft and xenograft reactions are fundamentally identical processes, and that the relative vigor of alloaggression may be explained by secondary potentiating mechanisms depending on species-specific interactions between aggressor and target cells.

scholarly journals Interleukin 10 deficiency attenuates induction of anti-TSH receptor antibodies and hyperthyroidism in a mouse Graves' model

2011 ◽  
Vol 209 (3) ◽  
pp. 353-357 ◽  
Author(s):  
Ikuko Ueki ◽  
Norio Abiru ◽  
Kentaro Kawagoe ◽  
Yuji Nagayama
Keyword(s):  
T Cell ◽  
Cell Function ◽  
Recombinant Adenovirus ◽  
Interleukin 10 ◽  
T Cell Response ◽  
Tsh Receptor ◽  
Mouse Strains ◽  
Susceptible Mouse ◽  
Ifn Γ

Experimental Graves'-like hyperthyroidism can be induced in susceptible mouse strains by repetitive immunizations with recombinant adenovirus expressing the human full-length TSH receptor (TSHR) or its A-subunit. Previous studies have shown that splenocytes from immunized mice produce interferon (IFN)-γ and interleukin (IL) 10 in response to antigen stimulation in an in vitro T cell recall assay. Although IFN-γ is now well known to be essential for disease induction, the role(s) played by IL10 are unknown. Therefore, this study was conducted to clarify the significance of endogenous IL10 in the pathogenesis of experimental Graves' disease using IL10 deficient (IL10−/−) mice. Our results show that T cell response was augmented when estimated by their antigen-specific secretion of the key cytokine IFN-γ, but B cell function was dampened, that is, anti-TSHR antibody titers were decreased in IL10−/− mice, resulting in a lower incidence of Graves' hyperthyroidism (54% in IL10+/+ vs 25% in IL10−/−). Thus, in addition to IFN-γ, these data clarified the role of IL10 for optimizing anti-TSHR antibody induction and eliciting Graves' hyperthyroidism in our Graves' mouse model.

scholarly journals Immunoregulatory circuits that modulate responsiveness to suppressor cell signal. Failure of B10 mice to respond to suppressor factors can be overcome by quenching the contrasuppressor circuit.

1981 ◽  
Vol 153 (6) ◽  
pp. 1547-1561 ◽  
Author(s):  
K Yamauchi ◽  
D R Green ◽  
D D Eardley ◽  
D B Murphy ◽  
R K Gershon
Keyword(s):  
T Cells ◽  
T Cell ◽  
Antibody Response ◽  
Sheep Erythrocyte ◽  
Biologically Active ◽  
Mouse Strains ◽  
Cellular Interactions ◽  
Spleen Cells ◽  
Suppressor Factor

The in vitro antibody response of spleen cells from B10 strain mice is not suppressed by factor preparations made by primed Ly-2 T cells, although these preparations can suppress the in vitro antibody response of spleen cells from other mouse strains (1-3)2. The factor preparations from Ly-2 cells contain at least two separable activities: one that acts as a suppressor moiety (Ly-2 T cell suppressor factor [Ly-2 TsF]) and a second factor that acts as an inducer of contrasuppression (Ly-2 TcsiF); the latter initiates a series of cellular interactions that leads to the inhibition of suppression that we refer to as contrasuppression. Removal of components (either cellular or humoral) of the contrasuppressor circuit makes spleen cells from B10 strain mice as easily suppressible as are those of other mouse strains. Thus, removal of the contrasuppressor inducer cell and/or its biologically active product with the use of an anit-J serum, or removal of the functional acceptor of the inducer cell with the same or other (Ly-2; Qa-1) antisera breaks the B10 suppressor barrier. Contrasuppressive activity. but not helper activity can be eluted from anit-I-J immunoabsorbents. The addition of B10 T cells to either B6 or B10 spleen cell culture deprived of acceptor cells for the TcsiF reconstitutes contrasuppression more efficiently than does the addition of C57BL/6 T cells. Ly-2 TcsiF is more cross-reactive than is Ly-2 TsF so that absorption of factor preparations from sheep erythrocyte-primed Ly-2 cells with horse erythrocytes also breaks the B10 suppressor barrier. The hyperresponsiveness of splenic T cells from B10 strains to Ly-2 TcsiF may be an in vitro exaggeration of a normal in vivo process. Thus it is possible that one can take advantage of this unusual situation to help dissect out the cellular and subcellular components of T cell circuits that moldulate sensitivity to immunoregulatory signals.

scholarly journals Immune responses induced by a Leishmania (Leishmania) amazonensis recombinant antigen in mice and lymphocytes from vaccinated subjects

1997 ◽  
Vol 39 (2) ◽  
pp. 71-78 ◽  
Author(s):  
Ana Paula FERNANDES ◽  
Elizabeth Cortez HERRERA ◽  
Wilson MAYRINK ◽  
Ricardo T. GAZZINELLI ◽  
Wen Yu LIU ◽  
...  
Keyword(s):  
Cutaneous Leishmaniasis ◽  
Recombinant Antigen ◽  
Leishmania Amazonensis ◽  
Mouse Strains ◽  
Susceptible Mouse ◽  
Blood Leukocytes ◽  
Th1 Cell ◽  
American Cutaneous Leishmaniasis ◽  
Antigenic Properties

In the search for Leishmania recombinant antigens that can be used as a vaccine against American Cutaneous Leishmaniasis, we identified a Leishmania (Leishmania) amazonensis recombinant protein of 33 kD (Larp33) which is recognized by antibodies and peripheral blood leukocytes (PBL) from subjects vaccinated with Leishvacin ®, Larp33 was expressed in Escherichia coli after cloning of a 2,2 kb Sau3A digested genomic fragment of L. (L.) amazonensis into the pDS56-6 His vector. Immunoblotting analysis indicated that Larp33 corresponds to an approximately 40-kD native protein expressed in promastigotes of L.(L.) amazonensis and L. (Viannia) braziliensis. Northern blots of total RNA also demonstrated that the gene coding for this protein is expressed in promastigotes of the major lineages of Leishmania causing American Cutaneous Leishmaniasis. Larp33 induced partial protection in susceptible mouse strains (BALB/c and C57BL/10) against L. (L.) amazonensis after vaccination using Bacille Calmette-Guerin (BCG) as adjuvant. In vitro stimulation of splenocytes from BALB/c protected mice with Larp33 elicited the secretion of IL-2 and IFN-<FONT FACE="Symbol">g</font>, suggesting that a Th1 cell-mediated protective response is associated with the resistance observed in these mice. As revealed by its immunogenic and antigenic properties, this novel recombinant antigen is a suitable candidate to compose a vaccine against cutaneous leishmaniasis

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