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1.
J Adv Nurs ; 2024 Sep 15.
Artigo em Inglês | MEDLINE | ID: mdl-39278630

RESUMO

AIM: To evaluate whether Preparedness Assessment for the Transition Home (PATH), a validated instrument assessing gaps in caregiver commitment and capacity to care for a patient with a disabling condition, would be helpful to identify gaps in preparing primary caregivers of patients with glioblastoma multiforme (GBM). DESIGN: A descriptive survey design with quantitative and qualitative data. METHODS: Former primary caregivers of patients with GBM were invited to complete a 17-question online survey during February and March 2023. Former caregivers, each having completed their caregiver journeys, are able to offer a unique perspective across the illness trajectory. Participants reviewed a copy of the PATH instrument and (a) responded to questions rating PATH helpfulness at each stage of the illness trajectory and (b) provided open-ended feedback on the instrument. RESULTS: One hundred seventeen of the 124 participants reported the PATH instrument would be helpful across all stages of the illness trajectory. While there were no statistically significant differences across the illness phases, response trends indicated using the PATH instrument earlier in the illness trajectory would have been more helpful to them as caregivers. Qualitative thematic analysis feedback indicated the most significant gap caregivers faced was education on the effects of the illness and treatment. CONCLUSION: It is vitally important to prepare and support caregivers. A validated instrument can identify unmet needs and inform care decisions. IMPLICATIONS FOR THE PROFESSION: Patient discharge plans should be guided by the needs and preferences of patients and caregivers. Identifying gaps in education and preparedness early in the illness trajectory may inform the care team of unmet needs, allowing them to tailor resources and support to improve outcomes for patients with GBM and their caregivers. IMPACT: Patient discharge plans should be guided by the needs and preferences of patients and caregivers. Identifying gaps in education and preparedness early in the illness trajectory may inform the care team of unmet needs, allowing them to tailor resources and support to improve outcomes for patients with GBM and their caregivers. PATH has the potential to inform healthcare professionals to develop customised care plans including education, resources and support for caregivers and patients with life-threatening illness. REPORTING METHOD: Study adheres to the STROBE reporting method. PATIENT OR PUBLIC CONTRIBUTION: Prior to deploying the survey to study participants, in addition to testing by study collaborators (authors), the survey was tested and feedback was received from graduate students and from administrators of the private Facebook group where the survey was promoted to study participants.

2.
Mar Drugs ; 22(1)2023 Dec 19.
Artigo em Inglês | MEDLINE | ID: mdl-38276642

RESUMO

Marine algae extracts are an important area of potential drug discovery; however, nearly all studies to date have used non-fluorescent-based methods to determine changes in target cell activity. Many of the most robust immunological and cellular analyses rely on fluorescent probes and readouts, which can be problematic when the algae extract is fluorescent itself. In this study, we identified the fluorescent spectrum of an isolated extract from the marine dinoflagellate Karenia brevis, which included two fluorescing components: chlorophyll α and pheophytin α. When excited at 405 nm and 664 nm, the extract emitted fluorescence at 676 nm and 696 nm, respectively. The extract and its fluorescing components, chlorophyll α and pheophytin α, entered phagocytic RAW 264.7 macrophages and non-phagocytic Vero kidney cells through distinct mechanisms. When incubated with the extract and its main components, both the RAW 264.7 macrophages and the Vero cells accumulated fluorescence as early as 30 min and continued through 48 h. Vero kidney cells accumulated the K. brevis fluorescent extract through a dynamin-independent and acidified endosomal-dependent mechanism. RAW 264.7 macrophages accumulated fluorescent extract through a dynamin-independent, acidified endosomal-independent mechanism, which supports accumulation through phagocytosis. Furthermore, RAW 264.7 macrophages downregulated cell-surface expression of CD206 in response to extract stimulation indicating activation of phagocytic responses and potential immunosuppression of these immune cells. This study represents the first characterization of the cellular update of K. brevis extracts in phagocytic versus non-phagocytic cells. The data suggest the importance of understanding cellular uptake of fluorescing algae extracts and their mechanism of action for future drug discovery efforts.


Assuntos
Dinoflagellida , Feofitinas , Animais , Chlorocebus aethiops , Camundongos , Células Vero , Feofitinas/metabolismo , Macrófagos/metabolismo , Fagocitose , Dinoflagellida/metabolismo , Dinaminas/metabolismo , Células RAW 264.7
3.
BMJ Open ; 14(3): e081783, 2024 Mar 12.
Artigo em Inglês | MEDLINE | ID: mdl-38479741

RESUMO

OBJECTIVES: To analyse the content of letters written by female spouse primary caregivers of patients with glioblastoma multiforme (GBM), a devastating and terminal primary brain cancer, and give voice to their experiences for medical providers of patients with GBM. DESIGN: A qualitative study using reflexive thematic analysis of letters written by female spouses/life partners and primary caregivers of patients with GBM. PARTICIPANTS: 101 current or former female spouse primary caregivers of patients with GBM wrote letters to share with the medical community between July 2019 and August 2019. INCLUSION CRITERIA: (1) the primary caregiver who is a spouse of a patient with glioblastoma, (2) be a member of the secret Facebook group, 'We are the wives of GBM and this is our story', and (3) completed informed consent for the contents of their letter to be included for primary and secondary data analysis. Participants who wrote letters but did not complete the informed consent were excluded from the study. RESULTS: Themes from the letters included the patient experiences: (1) medical details of the disease trajectory, (2) interactions of the patient/caregiver dyads with healthcare and (3) the changing patient condition over time. Themes focused on the caregiver experiences: (1) caregiver challenges, (2) caregiver responses and (3) caregiver coping strategies, and description of tangible needs that would help other caregivers in the future. Caregiver needs were highest during the living with disease progression phase. Caregivers wanted more education and to be valued as members of the care team. CONCLUSION: Shared decision-making through family-centred care would be beneficial for primary caregivers of patients with GBM. These findings provide opportunities to guide more timely and tailored interventions to provide support and improve care for patient/caregiver dyads to help mitigate the burden of this progressive disease and improve quality of life for caregivers.


Assuntos
Glioblastoma , Mídias Sociais , Humanos , Feminino , Cônjuges , Cuidadores , Glioblastoma/terapia , Qualidade de Vida , Grupos de Autoajuda
4.
Sci Signal ; 5(211): ra13, 2012 Feb 14.
Artigo em Inglês | MEDLINE | ID: mdl-22337809

RESUMO

In response to ligand binding to the Toll-like receptor 4 (TLR4) and myeloid differentiation-2 (MD-2) receptor complex, two major signaling pathways are activated that involve different adaptor proteins. One pathway depends on myeloid differentiation marker 88 (MyD88), which elicits proinflammatory responses, whereas the other depends on Toll-IL-1 receptor (TIR) domain-containing adaptor inducing interferon-ß (TRIF), which elicits type I interferon production. Here, we showed that the TLR4 agonist and vaccine adjuvant CRX-547, a member of the aminoalkyl glucosaminide 4-phosphate (AGP) class of synthetic lipid A mimetics, displayed TRIF-selective signaling in human cells, which was dependent on a minor structural modification to the carboxyl bioisostere corresponding to the 1-phosphate group on most lipid A types. CRX-547 stimulated little or no activation of MyD88-dependent signaling molecules or cytokines, whereas its ability to activate the TRIF-dependent pathway was similar to that of a structurally related inflammatory AGP and of lipopolysaccharide from Salmonella minnesota. This TRIF-selective signaling response resulted in the production of substantially less of the proinflammatory mediators that are associated with MyD88 signaling, thereby potentially reducing toxicity and improving the therapeutic index of this synthetic TLR4 agonist and vaccine adjuvant.


Assuntos
Proteínas Adaptadoras de Transporte Vesicular/metabolismo , Glucosamina/análogos & derivados , Compostos Organofosforados/farmacologia , Transdução de Sinais/efeitos dos fármacos , Receptor 4 Toll-Like/agonistas , Transporte Ativo do Núcleo Celular/efeitos dos fármacos , Proteínas Adaptadoras de Transporte Vesicular/genética , Western Blotting , Linhagem Celular , Linhagem Celular Tumoral , Núcleo Celular/efeitos dos fármacos , Núcleo Celular/metabolismo , Células Cultivadas , Quimiocina CCL5/metabolismo , Quimiocina CXCL10/metabolismo , Relação Dose-Resposta a Droga , Endocitose/efeitos dos fármacos , Glucosamina/química , Glucosamina/farmacologia , Células HEK293 , Humanos , Hidrazonas/farmacologia , Lipídeo A/farmacologia , Estrutura Molecular , Mutação , Fator 88 de Diferenciação Mieloide/genética , Fator 88 de Diferenciação Mieloide/metabolismo , NF-kappa B/metabolismo , Compostos Organofosforados/química , Estereoisomerismo , Receptor 4 Toll-Like/metabolismo , Transfecção , Fator de Necrose Tumoral alfa/metabolismo
5.
J Immunol ; 179(7): 4857-66, 2007 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-17878385

RESUMO

Aside from being the precursors of the Ab-secreting cells, B cells are engaged in other immune functions such as Ag presentation to T cells or cytokine production. These functions may contribute to the pathogenic role of B cells in a wide range of autoimmune diseases. We demonstrate that B cells acquire the capacity to amplify IFN-gamma production by CD4 and CD8 T cells during the course of the Th1 inflammatory response to Toxoplasma gondii infection. Using the two following different strategies, we observed that B cells from T. gondii-infected mice, but not from naive mice, induce higher IFN-gamma expression by splenic host T cells: 1) reconstitution of B cell-deficient mice with B cells expressing an alloantigen different from the recipients, and 2) adoptive transfer of B and T cells into RAG-/- mice. In vitro assays allowing the physical separation of T and B cells demonstrate that Ag-primed B cells enhance IFN-gamma production by T cells in a contact-dependent fashion. Using an OVA-transgenic strain of T. gondii and OVA-specific CD4 T cells, we observed that the proinflammatory effect of B cells is neither Ag specific nor requires MHCII expression. However, TNF-alpha expressed on the surface of B cells appears to mediate in part the up-regulation of IFN-gamma by the effector T cells.


Assuntos
Linfócitos B/metabolismo , Interferon gama/biossíntese , Linfócitos T/metabolismo , Fator de Necrose Tumoral alfa/metabolismo , Animais , Apresentação de Antígeno/imunologia , Linfócitos B/imunologia , Quimiocina CCL3 , Quimiocina CCL4 , Quimiocinas CC/metabolismo , Feminino , Antígenos de Histocompatibilidade Classe II/imunologia , Inflamação/imunologia , Ativação Linfocitária/imunologia , Proteínas Inflamatórias de Macrófagos/metabolismo , Camundongos , Camundongos Knockout , Baço/imunologia , Baço/metabolismo , Linfócitos T/imunologia , Fator de Necrose Tumoral alfa/deficiência , Fator de Necrose Tumoral alfa/genética
6.
J Immunol ; 176(12): 7589-97, 2006 Jun 15.
Artigo em Inglês | MEDLINE | ID: mdl-16751405

RESUMO

TLRs expressed by a variety of cells, including epithelial cells, B cells, and dendritic cells, are important initiators of the immune response following stimulation with various microbial products. Several of the TLRs require the adaptor protein, MyD88, which is an important mediator for the immune response following Toxoplasma gondii infection. Previously, TLR9-mediated innate immune responses were predominantly associated with ligation of unmethylated bacterial CpG DNA. In this study, we show that TLR9 is required for the Th1-type inflammatory response that ensues following oral infection with T. gondii. After oral infection with T. gondii, susceptible wild-type (WT; C57BL/6) but not TLR9(-/-) (B6 background) mice develop a Th1-dependent acute lethal ileitis; TLR9(-/-) mice have higher parasite burdens than control WT mice, consistent with depressed IFN-gamma-dependent parasite killing. A reduction in the total T cell and IFN-gamma-producing T cell frequencies was observed in the lamina propria of the TLR9(-/-) parasite-infected mice. TLR9 and type I IFN production was observed by cells from infected intestines in WT mice. TLR9 expression by dendritic cell populations is essential for their expansion in the mesenteric lymph nodes of infected mice. Infection of chimeric mice deleted of TLR9 in either the hemopoietic or nonhemopoietic compartments demonstrated that TLR9 expression by cells from both compartments is important for efficient T cell responses to oral infection. These observations demonstrate that TLR9 mediates the innate response to oral parasite infection and is involved in the development of an effective Th1-type immune response.


Assuntos
Mucosa Intestinal/imunologia , Mucosa Intestinal/parasitologia , Tecido Linfoide/imunologia , Tecido Linfoide/parasitologia , Receptor Toll-Like 9/fisiologia , Toxoplasmose Animal/imunologia , Administração Oral , Animais , Células Apresentadoras de Antígenos/imunologia , Células Apresentadoras de Antígenos/metabolismo , Células Apresentadoras de Antígenos/patologia , Citocinas/antagonistas & inibidores , Citocinas/biossíntese , Regulação para Baixo/genética , Regulação para Baixo/imunologia , Feminino , Hematopoese/genética , Hematopoese/imunologia , Ileíte/genética , Ileíte/imunologia , Ileíte/parasitologia , Imunidade Inata/genética , Imunofenotipagem , Interferon beta/biossíntese , Mucosa Intestinal/patologia , Tecido Linfoide/patologia , Mesentério , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Endogâmicos CBA , Camundongos Knockout , Células Th1/imunologia , Células Th1/metabolismo , Células Th1/patologia , Receptor Toll-Like 9/deficiência , Receptor Toll-Like 9/genética , Toxoplasma/imunologia , Toxoplasma/metabolismo , Toxoplasmose Animal/genética , Toxoplasmose Animal/metabolismo , Toxoplasmose Animal/patologia
7.
Infect Immun ; 70(11): 6048-57, 2002 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-12379681

RESUMO

Human neutrophils are rescued from apoptosis following incubation with once-washed, fibroblast-derived Toxoplasma gondii tachyzoites. Both infected and uninfected neutrophils are rescued, implicating a soluble mediator. In this study we investigated the origin and identity of this soluble mediator. Neutrophils were incubated either with purified tachyzoites or with conditioned medium derived from T. gondii-infected human fibroblasts. Conditioned medium was found to be a potent stimulus that delayed neutrophil apoptosis up to 72 h, whereas purified and extensively washed tachyzoites had no effect. Delayed apoptosis correlated with up-regulation of the neutrophil antiapoptotic protein, Mcl-1, and the neutrophil interleukin 3 receptor alpha subunit (IL-3Ralpha), suggesting a role for granulocyte-macrophage colony-stimulating factor (GM-CSF). GM-CSF and granulocyte colony-stimulating factor (G-CSF) were measurable in conditioned medium by enzyme-linked immunosorbent assay. Neutralizing antibodies to GM-CSF and G-CSF were additive in abrogating delayed neutrophil apoptosis induced by conditioned medium. Inhibitors of Src family tyrosine kinases, G(i) proteins, phosphatidylinositol 3-kinase, p44(erk1) and p42(erk2) mitogen-activated protein kinases, and Jak2 kinases partially attenuated the effect of conditioned medium, consistent with a role for G-CSF and/or GM-CSF. Hence, delayed neutrophil apoptosis is mediated by GM-CSF and G-CSF secreted by T. gondii-infected human fibroblasts. This enhanced neutrophil survival may contribute to the robust proinflammatory response elicited in the T. gondii-infected host.


Assuntos
Apoptose , Fator Estimulador de Colônias de Granulócitos/biossíntese , Fator Estimulador de Colônias de Granulócitos e Macrófagos/biossíntese , Neutrófilos/fisiologia , Toxoplasma/fisiologia , Animais , Células Cultivadas , Meios de Cultivo Condicionados , Fibroblastos/metabolismo , Fibroblastos/parasitologia , Subunidades alfa Gi-Go de Proteínas de Ligação ao GTP/fisiologia , Humanos , Interleucina-12/biossíntese , Proteínas Quinases Ativadas por Mitógeno/fisiologia , Fosfatidilinositol 3-Quinases/fisiologia , Receptores de Interleucina-3/biossíntese
8.
Gastroenterology ; 127(1): 119-26, 2004 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-15236178

RESUMO

BACKGROUND & AIMS: The loss of homeostasis is a hallmark of inflammatory bowel disease. Oral infection of susceptible mice with Toxoplasma gondii results in an acute lethal ileitis characterized by increased interferon gamma, tumor necrosis factor alpha, and inducible nitric oxide synthase; homeostasis results from transforming growth factor beta production by intraepithelial lymphocytes. The synthetic oleanane triterpenoid 2-cyano-3,12-dioxooleana-1,9-dien-28-oic acid (CDDO) is a potent anti-inflammatory molecule previously shown in vitro to suppress the de novo synthesis of inducible nitric oxide synthase and to induce the transcription and activation of genes from the transforming growth factor beta signaling pathway. METHODS: We evaluated the immune response in the small intestine and by intraepithelial lymphocytes after a single intraperitoneal dose of CDDO at the time of T. gondii oral infection. We abrogated the homeostatic effects of CDDO by blocking transforming growth factor beta in vivo. RESULTS: CDDO acid prevented ileitis development through the global down-regulation of inflammatory cytokines and chemokines. Total transforming growth factor beta(1) production by the intraepithelial lymphocytes increased, as did Smad2 expression. Blocking transforming growth factor beta reversed CDDO-induced protection and prevented the up-regulation of Smad2 in the small intestine. CONCLUSIONS: CDDO acid is a novel anti-inflammatory molecule capable of preventing ileitis by activating the transforming growth factor beta signaling pathway in a pathogen-driven ileitis model. This could represent a new treatment of inflammatory bowel disease.


Assuntos
Anti-Inflamatórios não Esteroides/administração & dosagem , Ileíte/parasitologia , Ácido Oleanólico/análogos & derivados , Ácido Oleanólico/administração & dosagem , Toxoplasmose/complicações , Fator de Crescimento Transformador beta/efeitos dos fármacos , Animais , Citocinas/efeitos dos fármacos , Citocinas/imunologia , Regulação para Baixo/genética , Regulação para Baixo/imunologia , Feminino , Ileíte/prevenção & controle , Injeções Intraperitoneais , Linfócitos/efeitos dos fármacos , Linfócitos/imunologia , Camundongos , Modelos Animais , Transdução de Sinais/imunologia , Fator de Crescimento Transformador beta/fisiologia
9.
Eur J Immunol ; 34(4): 1059-67, 2004 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-15048716

RESUMO

Intraepithelial lymphocytes (IEL) play a key role in gut homeostasis and are critical effector cells preventing the inflammatory intestinal lesions induced in mice following oral infection with Toxoplasma gondii. In this intestinal inflammatory model, CD4(+) T lymphocytes from the lamina propria (LP) synergize with the infected enterocytes to secrete pro-inflammatory chemokines and cytokines. In this study, we assessed the mechanisms accounting for the ability of IEL to modulate the inflammatory activity of these cells. Adoptive transfer of IEL purified from wild-type mice, or CD154-,CD95L- or IL-10-deficient mice infected with T. gondii completely impairs the development of the lethal ileitis in recipient mice orally infected with T. gondii. Compared with unprimed IEL isolated from naive mice, the CD8 alpha beta TCR alpha beta subset of primed IEL, isolated from T. gondii-infected mice, secretes increased amount of TGF-beta. IEL interact with the LP CD4(+) T lymphocytes, down-regulate their production of inflammatory cytokines such as IFN-gamma and reduce their proliferative activity. These effects are linked to the secretion of TGF-beta and are correlated with a shift in the balance between Smad7/T-bet down-regulation and Smad2/Smad3 up-regulation in LP CD4(+) T lymphocytes.


Assuntos
Proteínas de Ligação a DNA/imunologia , Ileíte/imunologia , Inflamação/imunologia , Linfócitos T/imunologia , Transativadores/imunologia , Transferência Adotiva , Animais , Feminino , Ileíte/parasitologia , Immunoblotting , Inflamação/parasitologia , Mucosa Intestinal/imunologia , Mucosa Intestinal/parasitologia , Intestinos/imunologia , Intestinos/parasitologia , Camundongos , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Transdução de Sinais/imunologia , Proteínas Smad , Linfócitos T/parasitologia , Toxoplasma/imunologia , Toxoplasmose/imunologia , Fator de Crescimento Transformador beta/imunologia
10.
Gastroenterology ; 125(2): 491-500, 2003 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-12891552

RESUMO

BACKGROUND & AIMS: Toxoplasma gondii, an obligate intracellular parasite, can invade intestinal epithelial cells and elicit a robust Th1 immune response. In this model of intestinal inflammation, CD8(+) intraepithelial lymphocytes (IELs) secrete transforming growth factor (TGF)-beta, which appears necessary for the maintenance of homeostasis in the intestine. However, the mechanism responsible for the IEL migration to the inflamed intestine is still unclear. METHODS: An in vitro coculture cell system was used to quantify the IEL attraction by an infected intestinal epithelial cell line (m-IC(cl2)). We used CCR5-deficient mice to determine which chemokine receptor-chemokine interaction could be responsible for the recruitment of antigen-specific CD8(+) IELs to the small intestine for the promotion of parasite clearance and host recovery. RESULTS: We observed increased expression of several chemokine receptors (CCR1, CCR2, CCR5, CXCR3) in the infected ileum. In particular, CCR5 expression was markedly increased in antigen-primed CD8(+) IELs. Experiments using recombinant chemokines as well as blocking antibodies showed that macrophage inflammatory protein (MIP)-1alpha and MIP-1beta were critical for their homing. CD8(+) IELs isolated from CCR5-deficient mice (CCR5-/-), despite their high production of TGF-beta and overexpression of activation markers, were impaired in their ability to migrate in vitro to the m-IC(cl2) monolayer or in vivo to the inflamed intestine after adoptive transfer. CONCLUSIONS: Our data emphasize the biologic role of CCR5 as an important component in the migration of intraepithelial CD8(+) T cells and the regulation of the inflammatory response following parasite infection.


Assuntos
Linfócitos T CD8-Positivos/imunologia , Enterite/imunologia , Mucosa Intestinal/imunologia , Receptores CCR5/fisiologia , Toxoplasma/imunologia , Animais , Movimento Celular , Quimiocinas/genética , Quimiotaxia , Feminino , Camundongos , Camundongos Endogâmicos C57BL , RNA Mensageiro/análise , Receptores CCR5/genética , Receptores de Quimiocinas/genética , Toxoplasmose Animal/imunologia
11.
J Immunol ; 173(4): 2725-35, 2004 Aug 15.
Artigo em Inglês | MEDLINE | ID: mdl-15294991

RESUMO

The role of specific microbial Ags in the induction of experimental inflammatory bowel disease is poorly understood. Oral infection of susceptible C57BL/6 mice with Toxoplasma gondii results in a lethal ileitis within 7-9 days postinfection. An immunodominant Ag of T. gondii (surface Ag 1 (SAG1)) that induces a robust B and T cell-specific response has been identified and a SAG1-deficient parasite (Deltasag1) engineered. We investigated the ability of Deltasag1 parasite to induce a lethal intestinal inflammatory response in susceptible mice. C57BL/6 mice orally infected with Deltasag1 parasites failed to develop ileitis. In vitro, the mutant parasites replicate in both enterocytes and dendritic cells. In vivo, infection with the mutant parasites was associated with a decrease in the chemokine and cytokine production within several compartments of the gut-associated cell population. RAG-deficient (RAG1(-/-)) mice are resistant to the development of the ileitis after T. gondii infection. Adoptive transfer of Ag-specific CD4(+) effector T lymphocytes isolated from C57BL/6-infected mice into RAG(-/-) mice conferred susceptibility to the development of the intestinal disease. In contrast, CD4(+) effector T lymphocytes from mice infected with the mutant Deltasag1 strain failed to transfer the pathology. In addition, resistant mice (BALB/c) that fail to develop ileitis following oral infection with T. gondii were rendered susceptible following intranasal presensitization with the SAG1 protein. This process was associated with a shift toward a Th1 response. These findings demonstrate that a single Ag (SAG1) of T. gondii can elicit a lethal inflammatory process in this experimental model of pathogen-driven ileitis.


Assuntos
Antígenos de Protozoários/imunologia , Ileíte/parasitologia , Intestinos/patologia , Proteínas de Protozoários/imunologia , Toxoplasmose Animal/imunologia , Toxoplasmose Animal/patologia , Doença Aguda , Transferência Adotiva , Animais , Antígenos de Protozoários/genética , Citocinas/imunologia , Feminino , Proteínas de Homeodomínio/genética , Proteínas de Homeodomínio/imunologia , Ileíte/imunologia , Intestinos/parasitologia , Camundongos , Mutação , Proteínas de Protozoários/genética , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Toxoplasma/imunologia
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