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1.
J Parasitol ; 92(3): 531-8, 2006 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-16883996

RESUMO

Mice were fed ad libitum with a normal diet (25% protein) or low-protein diets (0-12.5% protein) for a wk and then infected with a nonlethal or lethal strain of Plasmodium yoelii, that is, blood stage infection. The same diet was continued until recovery. Mice fed with a normal diet showed severe parasitemia during nonlethal infection, but survived the infection. They died within 2 wk in the case of lethal infection. However, all mice fed with low-protein diets survived without apparent parasitemia (there were small peaks of parasitemia) in cases of both nonlethal and lethal strains. These surviving mice were found to have acquired potent innate immunity, showing the expansion of NK1.1 -TCRint cells and the production of autoantibodies during malarial infection. Severe combined immunodeficiency (scid) mice, which lack TCRint cells as well as TCRhigh cells, did not survive after malarial infection of lethal strain of P. yoelii, even when low-protein diets were given. These results suggest that low-protein diets enhanced innate immunity and inversely decreased conventional immunity, and that these immunological deviations rendered mice resistant against malaria. The present outcome also reminds us of our experience in the field study of malaria, in which some inhabitants eventually avoided contracting malaria even after apparent malarial infection.


Assuntos
Dieta com Restrição de Proteínas , Malária/imunologia , Malária/prevenção & controle , Plasmodium yoelii/imunologia , Animais , Imunofenotipagem , Fígado/citologia , Contagem de Linfócitos , Linfócitos/classificação , Linfócitos/imunologia , Camundongos , Camundongos Endogâmicos C57BL , Camundongos SCID , Parasitemia/imunologia , Parasitemia/prevenção & controle , Baço/citologia , Timo/citologia
2.
Anticancer Res ; 25(3B): 2085-90, 2005.
Artigo em Inglês | MEDLINE | ID: mdl-16161253

RESUMO

We have previously reported that sodium fluoride (NaF) showed slightly higher cytotoxicity against human oral tumor cell lines than normal human oral cells. Possible changes in the NaF sensitivity of three normal human oral cell types (gingival fibroblast HGF, pulp cell HPC, periodontal ligament fibroblast HPLF) during in vitro ageing were investigated in the present study. When these cells were subcultured at 1:4 split ratio every week, their saturation density declined with increasing population doubling level (PDL), and they ceased to divide when they reached 20 PDL. Mitochondrial function, evaluated by MTT stainability per cell basis, was elevated at the terminal phase. NaF dose-dependently reduced the viable cell number, but did not show any beneficial (growth promoting) effect (so-called "hormesis") at lower concentrations. NaF produced large DNA fragments, without induction of internucleosomal DNA fragmentation, possibly due to weak activation of caspases -3, -8 and -9. Higher concentrations of NaF were required to reduce the number of viable senescent cells than younger cells, indicating that cells become resistant to cytotoxicity of NaF with in vitro ageing.


Assuntos
Boca/citologia , Boca/efeitos dos fármacos , Fluoreto de Sódio/farmacologia , Processos de Crescimento Celular/efeitos dos fármacos , Células Cultivadas , Senescência Celular/efeitos dos fármacos , Criança , Fragmentação do DNA/efeitos dos fármacos , Cavidade Pulpar/citologia , Cavidade Pulpar/efeitos dos fármacos , Feminino , Fibroblastos/citologia , Fibroblastos/efeitos dos fármacos , Gengiva/citologia , Gengiva/efeitos dos fármacos , Humanos , Nucleossomos/efeitos dos fármacos , Ligamento Periodontal/citologia , Ligamento Periodontal/efeitos dos fármacos
3.
Anticancer Res ; 25(3B): 2033-8, 2005.
Artigo em Inglês | MEDLINE | ID: mdl-16158941

RESUMO

In search of compounds which show tumor-specific cytotoxic activity, two 3,5-dibenzoyl-1, 4-dihydropyridines (GB5, GB12) were found to show one or two orders higher cytotoxic activity against human tumor cell lines (squamous cell carcinoma HSC-2, HSC-3, submandibular gland carcinoma HSG, promyelocytic leukemia HL-60) than human normal cells (gingival fibroblast HGF, pulp cells HPC, periodontal ligament fibroblasts HPLF). GB5 and GB12 weakly induced several apoptosis-associated properties, such as internucleosomal DNA fragmentation, and activation of caspases -3, -8 and -9, in both HL-60 and HSC-2 cells. Western blot analysis showed that GB5 and GB12 transiently increased the expression of both anti-apoptotic protein (Bcl-2) and proapoptotic proteins (Bax and Bad) in HL-60 cells. ESR spectroscopy showed these compounds did not produce any detectable amount of radicals, nor scavenged superoxide (generated by hypoxanthine-xanthine oxidase reaction) or nitric oxide (generated by 1-hydroxy-2-oxo-3-(N-3-methyl-3-aminopropyl)-3-methyl-1-triazene), suggesting that the induction of cytotoxic action is not via a radical-mediated reaction. The present study suggests that GB5 and GB12 may induce non-apoptotic cell death in tumor cell lines.


Assuntos
Antineoplásicos/farmacologia , Di-Hidropiridinas/farmacologia , Apoptose/efeitos dos fármacos , Carcinoma de Células Escamosas/tratamento farmacológico , Linhagem Celular Tumoral , Ensaios de Seleção de Medicamentos Antitumorais , Fibroblastos/efeitos dos fármacos , Sequestradores de Radicais Livres/farmacologia , Células HL-60 , Humanos , Óxido Nítrico/metabolismo , Neoplasias da Glândula Submandibular/tratamento farmacológico , Superóxidos/metabolismo
4.
Anticancer Res ; 25(1A): 161-70, 2005.
Artigo em Inglês | MEDLINE | ID: mdl-15816534

RESUMO

To clarify the mechanisms by which hydroquinone (HQ; 1,4-benzenediol) produces apoptosis, HQ-induced cytotoxicity, intemucleosomal DNA fragmentation, activation of superoxide dismutase (SOD), expression of Mn and Cu/ZnSOD mRNA and activation of caspase-3, -8 and -9 were investigated in the human promyelocytic leukemic cell line HL-60. Electrophoresis and activity staining of the SOD-enriched fraction showed that HQ reduced MnSOD activation more than Cu/ZnSOD activation, suggesting that it induces mitochondrial dysfunction at an early stage of apoptosis. Furthermore, the expression of MnSOD mRNA was suppressed to a greater extent than that of Cu/ZnSOD mRNA, implying that HQ causes apoptosis by inhibiting MnSOD induction. Release of cytochrome c and activation of procaspase-3 and -9, but not of procaspase-8, occurred more rapidly (as early as 6 h) in HQ-treated cells, suggesting that HQ activates the intrinsic pathway of apoptosis. Addition of the antioxidant N-acetyl-L-cysteine (NAC) significantly reduced the cytotoxicity of HQ. At a concentration that was cytotoxic to 50% of the cells (approximately 0.05 mM), HQ activated caspase-3; this effect was reduced in the presence of NAC. Interestingly, higher concentrations of HQ (0.1-0.2 mM) caused direct cell death; however, when combined with 5 mM NAC, the activation of caspase-3 was strongly enhanced, suggesting the promotion of apoptosis. The activation of caspase-3 by HQ/NAC combinations suggests that NAC, a precursor of intracellular glutathione synthesis, acts as a co-catalyst during HQ-induced apoptosis.


Assuntos
Apoptose/efeitos dos fármacos , Hidroquinonas/farmacologia , Acetilcisteína/farmacologia , Antioxidantes/farmacologia , Fragmentação do DNA/efeitos dos fármacos , Interações Medicamentosas , Eletroforese em Gel de Ágar , Células HL-60 , Humanos , Isoenzimas , Nucleossomos/efeitos dos fármacos , Nucleossomos/genética , RNA Mensageiro/biossíntese , RNA Mensageiro/genética , Superóxido Dismutase/biossíntese , Superóxido Dismutase/genética , Superóxido Dismutase/metabolismo
5.
Anticancer Res ; 24(2B): 737-42, 2004.
Artigo em Inglês | MEDLINE | ID: mdl-15161020

RESUMO

A series of simple alpha, beta-unsaturated carbonyl compounds (1-26) was characterized for their cytotoxic profiles against oral human normal and tumor cells. Several cycloalkenones showed potent cytotoxic activities against human oral squamous cell carcinoma HSC-2 cell line. Among them, 4,4-dimethyl-2-cyclopenten-1-one (12) exhibited low cytotoxic activity against a normal human cell, gingival fibroblast HGF, and displayed higher tumor-specific cytotoxicity (SI value = CC50 (HGF)/CC50 (HSC-2) = 4.0). The cytotoxicities of the unsaturated lactones were moderately tumor-specific (SI = 1.5-1.9). Agarose gel electrophoresis showed that the induction of internucleosomal DNA fragmentation in human promyelocytic leukemia cell HL-60 is dependent on the structure of alpha, beta-unsaturated carbonyl compounds. Fluorometric protease assay showed that some, but not all compounds, activated the caspase 3 in a dose-dependent manner. All alpha, beta-unsaturated carbonyl compounds studied did not activate caspases 8 and 9. The cytotoxic activity of alpha, beta-unsaturated carbonyl compounds was profoundly reduced in the presence of N-acetylcysteine. The study suggests that the presence of a non sterically hindered Michael acceptor seems to be an essential structural requirement for the cytotoxic activity in alpha, beta-unsaturated ketones.


Assuntos
Alcenos/farmacologia , Carcinoma de Células Escamosas/tratamento farmacológico , Cetonas/farmacologia , Neoplasias Bucais/tratamento farmacológico , Alcenos/química , Caspases/metabolismo , Células Cultivadas , Fragmentação do DNA/efeitos dos fármacos , Ensaios de Seleção de Medicamentos Antitumorais , Ativação Enzimática , Células HL-60 , Humanos , Cetonas/química , Relação Estrutura-Atividade , Células Tumorais Cultivadas
6.
Anticancer Res ; 24(2B): 711-7, 2004.
Artigo em Inglês | MEDLINE | ID: mdl-15161016

RESUMO

A variety of beta-diketones were evaluated for their cytotoxic profiles against oral human normal and tumor cells. Among 22 compounds (BD1-22) tested, the cytotoxicity of 3-formylchromone (BD17) (CC50=7.8 microg/mL) against human oral squamous cell carcinoma (HSC-2) cells was higher than that of curcumin (CC50=23.6 microg/mL). Tumor cell-specific cytotoxicity was also detected in BD17 which exhibited little cytotoxic activity against a normal human cell, gingival fibroblast (HGF). (-)-3- (BD13) (CC50=21.7 microg/mL) and (+)-3-(Trifluoroacetyl)camphor (BD12) (CC50=29.7 microg/mL) are enantiomers and showed cytotoxicity comparable to curcumin and dibenzoylmethane (BD2) (CC50=22.5 microg/mL). BD13 did not induce DNA fragmentation in HL-60 cells nor activate caspase 3, 8 and 9 in both HL-60 and HSC-2 cells, regardless of the presence or absence of FeCl3. On the other hand, BD17 was found to induce apoptosis in HSC-2 and HL-60 cells, as judged by internucleosomal DNA fragmentation, caspase 3, 8 and 9 activation and dysfunction of mitochondrial membrane potential. The cytotoxic activity of BD13, BD17 and curcumin was significantly reduced by chelation with FeCl3. The tumor-specific cytotoxicity and apoptosis-inducing activity of BD17 against human tumor cells undoubtedly warrant further studies of its efficacy as a cancer chemotherapeutic agent.


Assuntos
Apoptose/efeitos dos fármacos , Cetonas/farmacologia , Caspases/metabolismo , Ensaios de Seleção de Medicamentos Antitumorais , Ativação Enzimática/efeitos dos fármacos , Células HL-60 , Humanos , Membranas Intracelulares/efeitos dos fármacos , Membranas Intracelulares/fisiologia , Isoenzimas , Potenciais da Membrana/efeitos dos fármacos , Mitocôndrias/efeitos dos fármacos , Mitocôndrias/fisiologia , Células Tumorais Cultivadas
7.
Anticancer Res ; 24(2B): 755-62, 2004.
Artigo em Inglês | MEDLINE | ID: mdl-15161023

RESUMO

Hydroxyketone chelators, deferiprone (HK1), maltol (HK3) and their related compounds (HK2, 4-8), were characterized for their cytotoxic profiles against oral human normal and tumor cells. Most hydroxyketones except HK6 showed relatively higher tumor-specific cytotoxicity. Deferiprone (HK1), which showed the highest tumor specificity, had 10 times higher cytotoxicity than maltol (HK3) in both human promyelocytic leukemia HL-60 and human oral squamous cell carcinoma HSC-2 cell lines. The cytotoxic activity of HK1 against HL-60 and HSC-2 cells was reduced in the presence of FeCl3, while that of HK3 was significantly increased by FeCl3. Agarose gel electrophoresis showed that HK1 induced internucleosomal DNA fragmentation in HL-60 cells, but the addition of FeCl3 inhibited the DNA fragmentation. HK3 did not induce DNA fragmentation in HL-60 cells, regardless of the presence or absence of FeCl3. In HSC-2 cells, HK1 and 3 did not induce DNA fragmentation in the presence or absence of FeCl3. Colorimetric protease assay showed that HK1 activated the caspase 3, 8 and 9 in HL-60 cells. On the other hand, HK3 did not activate the caspase 3, 8 and 9 in HL-60 cells, but activated the caspase 3 only slightly in the presence of FeCl3. HK1 and 3 also activated the caspase 3, 8 and 9 in HSC-2 cells, but to a lesser extent. The present study suggested that the antitumor activity of hydroxyketones may be modified by Fe3+ concentration.


Assuntos
Antineoplásicos/farmacologia , Quelantes/farmacologia , Cetonas/farmacologia , Piridonas/farmacologia , Pironas/farmacologia , Tropolona/análogos & derivados , Antineoplásicos/química , Carcinoma de Células Escamosas/tratamento farmacológico , Caspases/metabolismo , Linhagem Celular Tumoral , Quelantes/química , Fragmentação do DNA/efeitos dos fármacos , Deferiprona , Ensaios de Seleção de Medicamentos Antitumorais , Ativação Enzimática/efeitos dos fármacos , Células HL-60 , Humanos , Cetonas/química , Mimosina/farmacologia , Monoterpenos/farmacologia , Neoplasias Bucais/tratamento farmacológico , Relação Estrutura-Atividade , Tropolona/farmacologia
8.
Anticancer Res ; 23(5A): 3719-26, 2003.
Artigo em Inglês | MEDLINE | ID: mdl-14666669

RESUMO

We have recently found that millimolar concentrations of sodium fluoride (NaF) induced apoptotic cell death, characterized by caspase activation and DNA fragmentation, in tumor cell lines. This finding paved the way to investigating the interaction between NaF and the oral environment. As an initial step, we investigated redox compounds, metals and saliva, which may modify the cytotoxic activity of NaF against a human oral squamous cell carcinoma cell line (HSC-2). The minimum exposure time to NaF required for cytotoxicity induction was 8 hours. Noncytotoxic concentrations of antioxidants (sodium ascorbate, gallic acid, epigallocatechin gallate, chlorogenic acid, curcumin, superoxide dismutase, catalase), oxidants (hydrogen peroxide, sodium hypochlorite), metals (CuCl, CuCl2, FeCl2, FeCl3, CoCl2) or saliva neither protected against, nor enhanced the cytotoxic activity of NaF. Cytotoxic concentrations of these compounds produced somewhat additive, but not synergistic, effects on the cytotoxicity of NaF. ESR analysis demonstrated that NaF did not apparently change the radical intensity of sodium ascorbate and gallic acid, measured under alkaline conditions. During the cell death induction in human promyelocytic leukemia HL-60 cells by NaF, the consumption of glucose rapidly declined, followed by a decline in the consumption of major amino acids. The present study suggests that the cytotoxic activity of NaF is not regulated by the redox mechanism, but rather linked to the rapid decline in glucose consumption at early stage.


Assuntos
Antioxidantes/farmacologia , Metais/farmacologia , Oxidantes/farmacologia , Saliva/química , Fluoreto de Sódio/farmacologia , Aminoácidos/metabolismo , Carcinoma de Células Escamosas/tratamento farmacológico , Carcinoma de Células Escamosas/metabolismo , Linhagem Celular Tumoral , Interações Medicamentosas , Glucose/metabolismo , Células HL-60 , Humanos , Oxirredução
9.
Parasitol Int ; 52(4): 259-68, 2003 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-14665382

RESUMO

Plasmodium yoelii-infected erythrocytes were injected into mice with or without 6.5 Gy irradiation. This irradiation suppressed erythropoiesis and induced severe immunosuppression. However, these mice showed a rather delayed infection, suggesting that fresh erythrocytes may become malarial targets. In other words, malarial infection did not persist without newly generated erythrocytes in mice. We then examined erythropoiesis in the liver and bone marrow of mice with malaria. Surprisingly, erythropoiesis began in the liver. At this time, the serum level of erythropoietin (EPO) was prominently elevated and the EPO mRNA also became detectable in the kidney. Many clusters of red blood cells appeared de novo in the parenchymal space of the liver. These results revealed that malarial infection had a potential to induce the onset of hepatic erythropoiesis in mice.


Assuntos
Eritropoese/fisiologia , Fígado/fisiopatologia , Malária/fisiopatologia , Plasmodium yoelii , Animais , Modelos Animais de Doenças , Imuno-Histoquímica , Leucócitos Mononucleares/fisiologia , Fígado/patologia , Malária/sangue , Malária/patologia , Camundongos , Camundongos Endogâmicos C57BL , Parasitemia/imunologia , Parasitemia/fisiopatologia , Valores de Referência , Fatores de Tempo
10.
Parasitol Int ; 52(1): 61-70, 2003 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-12543148

RESUMO

Immunological states during human malarial infection were examined. In parallel with parasitemia and anemia, granulocytosis was induced in the blood of patients, especially those infected with Plasmodium (P.) falciparum. At that time, the level of lymphocytes remained unchanged or slightly increased in the blood. However, the distribution of lymphocyte subsets was modulated, showing that the proportion of CD56(+)T cells, CD57(+)T cells, and gammadeltaT cells (i.e. all unconventional T cells) had increased in patients infected with P. falciparum or P. vivax. This phenomenon occurred at the early phase of infection and disappeared in the course of recovery. The data from patients with multiple attacks of P. vivax infection showed that there was no augmentation of these responses. In adult cases, the increase in the proportion of unconventional T cells seemed to closely parallel disease severity. However, all these responses were weak in children, even those infected with P. falciparum. In conjunction with accumulating evidence from mouse malaria experiments, the present results suggest that the immunological state induced by malarial infection might mainly be an event of unconventional T cells and that the immunological memory might not be long-lasting, possibly due to the properties of unconventional T cells.


Assuntos
Células Matadoras Naturais/imunologia , Ativação Linfocitária , Malária Falciparum/imunologia , Malária Vivax/imunologia , Linfócitos T/imunologia , Adolescente , Adulto , Animais , Antígenos de Protozoários/imunologia , Antígenos de Superfície/imunologia , Biomarcadores/análise , Antígeno CD56/análise , Antígenos CD57/análise , Criança , Pré-Escolar , Feminino , Humanos , Imunidade Inata , Células Matadoras Naturais/química , Cinética , Masculino , Pessoa de Meia-Idade , Plasmodium falciparum/crescimento & desenvolvimento , Plasmodium vivax/crescimento & desenvolvimento , Subpopulações de Linfócitos T/classificação , Subpopulações de Linfócitos T/imunologia , Fatores de Tempo
11.
In Vivo ; 17(6): 583-91, 2003.
Artigo em Inglês | MEDLINE | ID: mdl-14758725

RESUMO

We investigated six endodontic agents for their ability to induce apoptosis and modify the cytotoxic activity of NaF against human squamous cell carcinoma (HSC-2) and human promyelocytic leukemia (HL-60) cell lines. Four Group I agents (Form Cresol, Cam Phenic, Eucaly Soft, GC Fuji Varnish), but not two Group II agents (Caviton, Canals-N), induced internucleosomal DNA fragmentation and activated caspases 3, 8 and 9 in HL-60 cells. Only Cam Phenic among these agents additively enhanced the cytotoxic activity of NaF in HSC-2 and HL-60 cells. Form Cresol and Cam Phenic reduced the glucose consumption at early stage, possibly due to their toxic effect. Amino acid analysis suggests that the higher cytotoxicity of Form Cresol may be derived, at least in part, from its oxidizing action.


Assuntos
Apoptose/efeitos dos fármacos , Carcinoma de Células Escamosas , Leucemia Promielocítica Aguda , Neoplasias Bucais , Fluoreto de Sódio/farmacologia , Sulfato de Cálcio/farmacologia , Caspase 3 , Caspase 8 , Caspase 9 , Caspases/metabolismo , Cimentos Dentários , Combinação de Medicamentos , Glucose/metabolismo , Células HL-60 , Humanos , Metionina/metabolismo , Higiene Bucal , Oxirredução , Materiais Restauradores do Canal Radicular , Compostos de Vinila/farmacologia , Óxido de Zinco/farmacologia
12.
Anticancer Res ; 23(6C): 4729-36, 2003.
Artigo em Inglês | MEDLINE | ID: mdl-14981920

RESUMO

We have recently found that sodium fluoride (NaF) induced apoptotic cell death in tumor cell lines. We investigated here whether 6 popular antitumor compounds modify the cytotoxic activity of NaF against human squamous cell carcinoma (HSC-2) and human promyelocytic leukemia (HL-60) cell lines. Cytotoxic concentrations of cisplatin, etoposide, doxorubicin or peplomycin (tentatively termed as Group I compounds), but not methotrexate and 5-FU (tentatively termed as Group II compounds), enhanced the cytotoxic activity of NaF. NaF and Group I compounds induced internucleosomal DNA fragmentation in HL-60 cells, whereas Group II compounds were inactive even in the presence of NaF. Most Group I compounds except doxorubicin (which induced DNA fragmentation less effectively than others) activated caspase 3 more efficiently than Group II compounds. Caspase 8 (involved in non-mitochondrial extrinsic pathway) and caspase 9 (involved in mitochondrial intrinsic pathway) were also activated, but to a much lesser extent. NaF reduced the glucose consumption at early stage, possibly by inhibition of glycolysis, whereas cisplatin and etoposide reduced the glucose consumption at later stage, suggesting that early decline of glucose consumption is rather specific to NaF.


Assuntos
Antineoplásicos/farmacologia , Apoptose/efeitos dos fármacos , Sobrevivência Celular/efeitos dos fármacos , Fluoreto de Sódio/toxicidade , Carcinoma de Células Escamosas , Cisplatino/toxicidade , Doxorrubicina/toxicidade , Etoposídeo/toxicidade , Fluoruracila/farmacologia , Glicólise/efeitos dos fármacos , Células HL-60 , Humanos , Cinética , Metotrexato/farmacologia , Peplomicina/toxicidade , Células Tumorais Cultivadas
13.
Eur J Immunol ; 32(9): 2551-61, 2002 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-12207339

RESUMO

Natural killer T (NKT) cells and CD5(+)B cells were searched for in various immune organs of autoimmune prone (NZBxNZW)F(1) (NZB/W F(1)) mice. The number of lymphocytes increased in the liver, spleen, and peritoneal cavity after the onset of disease (at the age of 30 weeks) while the number of thymocytes decreased at that time. Prominent changes of lymphocyte subsets were seen in the liver and peritoneal cavity, namely, expansion of IL-2Rbeta(+)TCRalpha beta(int) cells in the liver and of CD5(+)B220(+) cells in the peritoneal cavity. The majority of TCRalpha beta(int) cells in the liver were NK1.1(+), and CD5(+)B cells in the peritoneal cavity were CD1d(+). Proteinuria became prominent in NZB/W F(1) mice with the progression of disease. In parallel with this progression, the proportion of NKT cells decreased slightly in the liver, but their absolute number remained at a high level in this organ. These NKT cells were CD4(+) and used an invariant chain of Valpha14Jalpha281 for TCRalpha. Reflecting the elevation of CD5(+)B cells, autoantibodies against hepatocyte cytoplasmand denatured DNA were detected in sera. Although NKT cells are known to be immunoregulatory cells in some autoimmune mice, the present results raise the possibility that NKT cells as well as CD5(+)B cells might be associated with the onset of autoimmune diseases in NZB/W F(1) mice. Indeed, NKT cells in F(1) mice had a high potential to induce autoimmune-like inflammationwhen alpha-galactosylceramide was administered or when active NKT cells were transferred into young F(1) mice.


Assuntos
Doenças Autoimunes/imunologia , Subpopulações de Linfócitos B/imunologia , Antígenos CD4/análise , Antígenos CD5/análise , Células Matadoras Naturais/imunologia , Transtornos Linfoproliferativos/imunologia , Subpopulações de Linfócitos T/imunologia , Transferência Adotiva , Animais , Anticorpos Antinucleares/imunologia , Especificidade de Anticorpos , Antígenos CD1/análise , Antígenos CD1d , Autoanticorpos/imunologia , Doenças Autoimunes/patologia , Subpopulações de Linfócitos B/patologia , Cruzamentos Genéticos , Citoplasma/imunologia , DNA/imunologia , Progressão da Doença , Galactosilceramidas/imunologia , Galactosilceramidas/toxicidade , Hepatócitos/imunologia , Glomérulos Renais/patologia , Células Matadoras Naturais/patologia , Fígado/patologia , Contagem de Linfócitos , Transtornos Linfoproliferativos/patologia , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Endogâmicos MRL lpr , Camundongos Endogâmicos NZB , Cavidade Peritoneal/patologia , Proteinúria/etiologia , Proteinúria/patologia , Receptores de Antígenos de Linfócitos T alfa-beta/análise , Organismos Livres de Patógenos Específicos , Baço/patologia , Subpopulações de Linfócitos T/patologia , Subpopulações de Linfócitos T/transplante
14.
J Immunol ; 169(1): 301-6, 2002 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-12077258

RESUMO

Athymic nude mice carry neither conventional T cells nor NKT cells of thymic origin. However, NK1.1(-)TCR(int) cells are present in the liver and other immune organs of athymic mice, because these lymphocyte subsets are truly of extrathymic origin. In this study, we examined whether extrathymic T cells had the capability to protect mice from malarial infection. Although B6-nu/nu mice were more sensitive to malaria than control B6 mice, these athymic mice were able to survive malaria when a reduced number of parasitized erythrocytes (5 x 10(3) per mouse) were injected. At the fulminant stage, lymphocytosis occurred in the liver and the major expanding lymphocytes were NK1.1(-)TCR(int) cells (IL-2Rbeta(+)TCRalphabeta(+)). Unconventional CD8(+) NKT cells (V(alpha)14(-)) also appeared. Similar to the case of B6 mice, autoantibodies (IgM type) against denatured DNA appeared during malarial infection. Immune lymphocytes isolated from the liver of athymic mice which had recovered from malaria were capable of protecting irradiated euthymic and athymic mice from malaria when cell transfer experiments were conducted. In conjunction with the previous results in euthymic mice, the present results in athymic mice suggest that the major lymphocyte subsets associated with protection against malaria might be extrathymic T cells.


Assuntos
Fígado/imunologia , Malária/imunologia , Malária/prevenção & controle , Plasmodium yoelii/imunologia , Baço/imunologia , Subpopulações de Linfócitos T/imunologia , Transferência Adotiva , Animais , Autoanticorpos/biossíntese , Agregação Celular/imunologia , Ciclo Celular/imunologia , Imunofenotipagem , Células Matadoras Naturais/citologia , Células Matadoras Naturais/imunologia , Células Matadoras Naturais/patologia , Fígado/citologia , Fígado/patologia , Transplante de Fígado/imunologia , Contagem de Linfócitos , Linfocitose/imunologia , Malária/mortalidade , Malária/patologia , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Nus , Receptores de Antígenos de Linfócitos T alfa-beta/biossíntese , Baço/citologia , Baço/patologia , Análise de Sobrevida , Subpopulações de Linfócitos T/citologia , Subpopulações de Linfócitos T/patologia , Subpopulações de Linfócitos T/transplante , Timo/citologia , Timo/imunologia , Timo/patologia , Fatores de Tempo
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