Добірка наукової літератури з теми "Humoral and cellular immunity"

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Статті в журналах з теми "Humoral and cellular immunity":

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Colombo, Daniela, Alessandra Fritsch, Karen Gomes Ordovas, Allesandra Spode, and Maria Lucia Scroferneker. "Playing with cellular and humoral immunity." Biochemical Education 26, no. 1 (January 1998): 20–21. http://dx.doi.org/10.1016/s0307-4412(97)00140-4.

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Veien, N. K., F. Hardt, G. Bendixen, J. Genner, J. Ringsted, J. Wanstrup, A. Wiik, and E. Christiansen. "Humoral and Cellular Immunity in Sarcoidosis." Acta Medica Scandinavica 203, no. 1-6 (April 24, 2009): 321–26. http://dx.doi.org/10.1111/j.0954-6820.1978.tb14881.x.

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Kiilstra, Aize. "Ocular humoral immunity." Experimental Eye Research 55 (September 1992): 29. http://dx.doi.org/10.1016/0014-4835(92)90311-f.

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Maria Angeles Gomez Morales and Edoardo Pozio. "Humoral and Cellular Immunity Against Cryptosporidium Infection." Current Drug Target - Immune, Endocrine & Metabolic disorders 2, no. 3 (October 1, 2002): 291–301. http://dx.doi.org/10.2174/1568005310202030291.

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Angeles, M., G. Morales, and E. Pozio. "Humoral and Cellular Immunity Against Cryptosporidium Infection." Current Drug Targets-Immune, Endocrine & Metabolic Disorders 2, no. 3 (October 1, 2002): 291–301. http://dx.doi.org/10.2174/1568008023340505.

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Skovmann-Sørensen, O., H. Schrøder, Anné Møller-larsen, and S. Haahr. "Cellular and Humoral Immunity in Hodgkin's Disease." Scandinavian Journal of Haematology 27, no. 3 (April 24, 2009): 171–80. http://dx.doi.org/10.1111/j.1600-0609.1981.tb00469.x.

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NAKANISHI, Yoshinobu. "Humoral and Cellular Responses in Innate Immunity." YAKUGAKU ZASSHI 126, no. 12 (December 1, 2006): 1207–12. http://dx.doi.org/10.1248/yakushi.126.1207.

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Seledtsov, V. I., L. S. Litvinova, I. A. Seledtsova, E. V. Kirienkova, and V. V. Shupletsova. "HUMORAL AND CELLULAR IMMUNITY FACTORS IN MYOCARDIAL INFARCTION." Medical Immunology (Russia) 12, no. 6 (July 21, 2014): 477. http://dx.doi.org/10.15789/1563-0625-2010-6-477-484.

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Steelman, Samantha M., Daisy Johnson, Bettina Wagner, AshleyM Stokes, and Bhanu P. Chowdhary. "Cellular and humoral immunity in chronic equine laminitis." Veterinary Immunology and Immunopathology 153, no. 3-4 (June 2013): 217–26. http://dx.doi.org/10.1016/j.vetimm.2013.03.001.

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Dola, O. L. "The state of the immunity system in women with latent Papillomavirus infection of the cervix." HEALTH OF WOMAN, no. 7(123) (September 30, 2017): 135–38. http://dx.doi.org/10.15574/hw.2017.123.135.

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The article presents modern aspects of the state of immunity in women with latent papillomavirus infection (PVI) of the cervix. The objective: the study of the indicators characterizing the state of immunity in women with latent PVI of the cervix, often associated with urogenital infections (UGI), at the beginning of the survey and after 6 months of observation. Patients and methods. The study of cellular and humoral immunity was performed in 210 women with latent papillomavirus infection (PVI) and 15 healthy women at the beginning of the examination and 6 months later. 84 women were diagnosed with a monoinfection, 126 had a combined PVI and a urogenital infection (UGI). In 140 women transient PVI is established, in 70 – persistent. Results. In women with latent cervical pylori cervix, disorders of cellular immunity were observed (a slight decrease in the relative amount of CD3+, CD4+ lymphocytes and a simultaneous increase in the number of CD8+ lymphocytes, natural killers and B-lymphocytes) against the background of activation of the humoral immunity unit. Nonspecific protection of the female body with PVI was characterized by inhibition of the phagocytic reaction of neutrophils (Nf) and monocytes (Mg) against the background of an increase in oxygen-dependent metabolism, primarily HF, and a decrease in the functional reserve for both NF and MZ. The most pronounced disorders were found for patients with combined PVI and UGI. Conclusion. In women with transient PVI normalization of cellular and humoral immunity was observed, and the further persistence of the human papillomavirus in the genitals led to a more significant inhibition of phagocytic and HCT activity of phagocytes, as well as to a decrease in some parameters of the cellular and humoral immunity units. Key words: papillomavirus infection, cervix, cellular and humoral immunity.

Дисертації з теми "Humoral and cellular immunity":

1

Tran, Mai Hue. "Investigations of humoral and cellular immune responses directed against MUCI epithelial mucin in ovarian and breast carcinoma /." St. Lucia, Qld, 2002. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe17997.pdf.

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SILVA, Fabiana Leticia da. "Efeitos da amamentação em camundongos esquistossomóticos na imunidade anti-ovalbumina de descendentes adultos deficientes na produção das citocinas IL-12/IL-23." Universidade Federal de Pernambuco, 2014. https://repositorio.ufpe.br/handle/123456789/17158.

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O contato prévio com o leite de mães esquistossomóticas induziu, em camundongos adultos, potencialização da produção de anticorpos e aumento da capacidade de apresentação de antígeno pelos linfócitos B, em resposta ao antígeno heterólogo ovalbumina (OVA). Considerando a imunização com OVA um modelo vacinal, as reações inflamatórias e a produção de anticorpos em resposta a esse antígeno são importantes para o desenvolvimento de uma imunidade satisfatória do hospedeiro. Nesse sentido, as células Th1 e Th17 são importantes fatores para o desenvolvimento dessas respostas. Dessa forma, os camundongos deficientes na produção de IL-12/IL-23 (12p40 knockout-KO) são predispostos a desenvolverem uma resposta Th2 polarizada, tornando-se menos responsivos às vacinações. Diante disso, o presente trabalho investigou o efeito da amamentação em mães infectadas pelo Schistosoma mansoni sobre as imunidades humoral e celular de camundongos adultos C57BL/6 12p40 KO, em resposta ao modelo vacinal acima citado. Foram avaliados: a cinética das reações de hipersensibilidade in vivo; os níveis plasmáticos das imunoglobulinas IgG1 e IgG2a; a produção das citocinas IFN-γ, IL-17, IL-5, IL-6, IL-10 e TGF- pelas células esplênicas e a reação inflamatória provocada no coxim plantar. Para isso, camundongos machos, deficientes na produção de IL-12 e IL-23 (IL-12p40 KO) e camundongos selvagens (wild-type/WT) foram divididos nos seguintes grupos: camundongos IL-12p40 KO amamentados em mães infectadas (AI IL-12p40 KO); camundongos IL-12p40 KO amamentados em mães sem infecção (NANI IL-12p40 KO); camundongos selvagens amamentados em mães infectadas (AI WT) e camundongos selvagens amamentados em mães sem infecção (NANI WT). Cinquenta por cento dos animais de cada grupo foram imunizados com OVA em adjuvante. Os outros 50% porcento restantes permaneceram sem imunização. No grupo AI WT houve aumentado de produção de IgG2a, IL-5, TGF-β e IL-6, com baixos níveis de IL-17, em comparação ao NANI WT. Nos animais AI IL-12p40 KO, a produção de IgG2a, IL-5 e TGF-β foi mais alta do que o grupo NANI IL-12p40 KO e similar ao grupo AI WT, mas a produção de IL-6 foi mais baixa. O grupo AI WT mostrou intenso infiltrado inflamatório de eosinófilos na reação de hipersensibilidade tardia (RHT), com acentuado edema em comparação com o edema menos intenso e infiltrado inflamatório de neutrófilos do grupo NANI WT. Os animais NANI IL-12p40 KO e AI IL-12p40 KO não apresentam RHT, porém a reação inflamatória no AI IL-12p40 KO foi menos intensa que nos NANI IL-12p40 KO. Em conclusão, o contato com antígenos do parasito, através da amamentação, induziu, no descendente adulto, uma melhor resposta de anticorpo neutralizante, mesmo diante da deficiência na produção de IL-12e IL-23. Nesta condição, embora tenha havido uma notável produção de IL-5, a lactação em mães infectadas atenuou a reação inflamatória, provavelmente através da regulação cruzada entre TGF-β e IL-6, modulando, desta forma, o status de hiperativação desses animais.
The previous contact with mothers milk schistosomiasis induced in adult mice enhancement of antibody production and increased antigen presentation capacity by B lymphocytes in response to the heterologous antigen ovalbumin (OA). Considering immunization with OA one vaccine model, inflammatory reactions and antibody production in response to antigen are important for the development of a suitable host immunity. In this sense, the Th1 and Th17 cells are important factors for the development of these responses. Thus, mice deficient in IL-12/IL-23 (12p40 knockout-KO) are likely to develop a polarized Th2 response, making it less responsive to vaccination. Therefore, the present study investigated the effect of breastfeeding in mothers infected with Schistosoma mansoni on the humoral and cellular adult C57BL/6 12p40 KO in response to vaccination model mentioned above. Were evaluated: the kinetics of in vivo hypersensitivity reactions; plasma levels of IgG1 and IgG2a immunoglobulins; the production of the cytokines IFN-γ, IL-17, IL-5, IL-6, IL-10 and TGF-β by spleen cells and the inflammatory reaction induced in the footpad. To this end, male mice deficient in IL-12 and IL-23 (IL-12p40 KO) and wild-type mice (Wild-type/WT) were divided into the following groups: IL-12p40 KO mice suckled by infected mothers (IL-12p40 KO- SIM); IL-12p40 KO mice suckled by uninfected mothers (IL-12p40 KO); Wild-type mice suckled by infected mothers (SIM) and wild-type mice suckled by uninfected mothers (CONTROL). Fifty percent of animals in each group were immunized with OA in adjuvant. The other 50% remaining percent remained without immunization. In the SIM group was increased production of IgG2a, IL-5, TGF-β and IL-6, IL-17 with low levels compared to CONTROL. In animals IL-12p40 KO-SIM the production of IgG2a, IL-5 and TGF-β was higher than the IL-12p40 KO similar to group SIM, but IL-6 production was lower. The SIM group showed intense inflammatory infiltrate of eosinophils in the delayed hypersensitivity reaction (DTH), with severe edema compared with the less intense edema and inflammatory infiltration of neutrophils CONTROL group. The animals IL-12p40 KO and IL-12p40KO-SIM not have DTH, but the inflammatory reaction in the IL-12p40KO-SIM was less intense than in IL-12p40 KO. In conclusion, contact with parasite antigens, through breastfeeding, induced in adult offspring, better neutralizing antibody response, despite the deficiency in the production of IL-12 and IL-23. In this condition, though there has been a remarkable IL-5 production in lactating mothers infected with attenuated inflammatory response, probably via cross regulation between TGF-β and IL-6 modulate thereby the status of hyperactivation of these animals.
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Santos, Liliane Almeida Carneiro. "Estudo prospectivo sobre a dinâmica da evolução clínica e imunológica da infecção canina por Leishmania (Leishmania) infantum chagasi em área endêmica de leishmaniose visceral no estado do Pará." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/10/10133/tde-27102016-142051/.

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Leishmaniose visceral canina (LVC) é um dos problemas de saúde pública mais importantes da América Latina, pois geralmente precede a doença humana, a leishmaniose visceral americana (LVA), causada pela Leishmania (L.) infantum chagasi. No presente estudo prospectivo analisou-se durante período de dois anos a prevalência, incidência e dinâmica da evolução clínico-imunológica da infecção canina pela L. (L.) i. chagasi em uma coorte de 316 cães mestiços que vivem em área endêmica de LVA no município de Barcarena, Pará, Amazônia Brasil, pelo uso combinado do teste de imunofluorescência indireta (RIFI-IgG) e de hipersensibilidade tardia (RIM), bem como a pesquisa do parasita pela aspiração do linfonodo poplíteo para o diagnóstico da infecção. A reatividade para RIFI e RIM reconheceu três diferentes perfis de resposta imunológica: (I) RIFI (+) / RIM (-) (81 cães), (II) RIFI (-) / RIM (+) (17 cães), e (III) RIFI (+) / RIM (+) (13 cães), proporcionando uma prevalência global da infecção de 35,1% (111/316). Desta forma, a prevalência específica do perfil I (25,6%) foi superior as dos perfis II e III, 5,4% e 4,1%, respectivamente. Além disso, a frequência destes perfis entre 111 cães infectados mostrou que a taxa de 73% do perfil I também foi maior do que os dos perfis II (15,3%) e III (11,7%). A prevalência da infecção de acordo com as faixas etárias revelou que a taxa de 27,5% do grupo ≥1ano <7 anos foi maior do que as de <1 ano (5,3%) e ≥7anos (2,2%), respectivamente. Por outro lado, a incidência global da infecção foi de 5,7% cães / mês (5,4% perfil I, 0,3% perfil II e 0,0% perfil III). No entanto, observou-se uma progressiva diminuição nas taxas de incidência nos seguintes pontos de tempo: seis (3,6% cães / mês), doze (1,7% cães / mês) e vinte e quatro (0,4% cães / mês) meses do estudo. Além disso, a incidência da infecção de acordo com os grupos etários demonstraram que a taxa de 6,6% cães / mês no grupo <1 ano foi maior em comparação com as de 5,3% e 3,3% cães / mês nos grupos ≥1ano e <7 anos, e <1 ano, respectivamente. O diagnóstico parasitológico da infecção foi confirmado em 19% (21/111) no estudo da prevalência, sendo a maioria dos cães (85,7%) do perfil I, onde 61,1% eram sintomáticos e 38,9% assintomáticos. Entre o restante (14,3%), o diagnóstico foi associado ao perfil III, sendo 66,6% assintomáticos e 33,3% sintomáticos. No levantamento da incidência, o diagnóstico foi confirmado em 11% dos cães, todos pertencentes ao perfil I, sendo 60% assintomáticos e 40% sintomáticos. Com relação ao estado clínico de todos os 179 cães diagnosticados infectados durante o período de dois anos, observou-se que entre 145 (81%) cães do perfil I, 82% eram assintomáticos e 18% sintomáticos; entre os 21 (11,7%) cães do perfil II, todos (100%) eram assintomáticos; e entre 13 (7,3%) cães do perfil III, 84,6% eram assintomáticos e 15,4% sintomáticos. Além disso, observou-se que a conversão do estado clínico assintomático ao sintomática foi registado principalmente em cães do perfil I (40,2%) do que aqueles dos perfis II (5,8%) e III (9%). Por outro lado, apenas 3,2% dos cães do perfil I [RIFI (+) / RIM (-)] converteu resposta RIM (+), enquanto 80% de cães do perfil II [RIFI (-) / RIM (+)] converteu resposta RIFI (+). Por fim, demonstrou-se que 100% dos óbitos por LVC ocorreu entre os cães do perfil I, sendo 85,7% na prevalência e 14,3% na incidência. Considerando todos esses resultados, parece razoável que a interação entre parasita e resposta imune canina é suportada principalmente pelo perfil imunológico claramente vulnerável, o perfil I [RIFI (+) / RIM (-)], o qual não oferece qualquer resistência ao parasita, tornando o cão altamente susceptível à infecção
Canine visceral leishmaniasis (CVL) is one of the most important public health problems in Latin America because it usually precedes human disease, American visceral leishmaniais (AVL), being caused by Leishmania (L.) infantum chagasi. In the present prospective study it was analyzed during two years period the prevalence, incidence and dynamics of the clinical-immunological evolution of canine L. (L.) i. chagasi-infection in a cohort of 316 mongrel dogs living in endemic area of AVL in Barcarena municipality, Pará State, Amazonian Brazil, by the combined use of the indirect fluorescence antibody test (IFAT-IgG) and delayed-type hypersensitivity (DTH), as well as the parasite research by the popliteal lymph node aspiration for the diagnosis of infection. The IFAT and DTH reactivity recognized three different immune response profiles: (I) IFAT(+)/DTH(-) (81 dogs), (II) IFAT(-)/DTH(+) (17 dogs), and (III) IFAT(+)/DTH(+) (13 dogs), providing an overall infection prevalence of 35,1% (111/316). In this way, the specific prevalence of profile I 25,6% was higher than those of profiles II 5,4% and III 4,1%. Moreover, the frequency of these profiles among 111 infected dogs showed that the rate 73% of profile I was also higher than those of profiles II 15,3% and III 11,7%. The infection prevalence according to the age groups revealed that the rate 27,5% of ≥1year <7years was higher than those of <1year 5,3% and ≥7years 2,2%, respectively. On the other hand, the overall incidence of infection was 5,7% dogs/month (5,4% profile I, 0,3% profile II and 0,0% profile III). However, it was noted a progressive decreasing in the incidence rates at the following time-points: six (3,6% dogs/month), twelve (1,7% dogs/month) and twenty four (0,4% dogs/month) months of the study. In addition, the infection incidence according to the age groups demonstrated that the rate 6,6% dogs/month of <1year was higher compared to those of 5,3% and 3,3% dogs/month of ≥1year and <7years, and <1year, respectively. The parasitological diagnosis of infection was confirmed in 19% (21/111) at the prevalence survey, being most dogs (85,7%) of the profile I, 61,1% symptomatic and 38,9% asymptomatic ones. Among the remainder 14,3%, the diagnosis was associated to the profile III, 66,6% in asymptomatic and 33,3% in symptomatic dogs. At the incidence survey, the diagnosis was confirmed in 11% of dogs, all from the profile I, 60% asymptomatic and 40% symptomatic ones. With regards to clinical status of all 179 infected dogs diagnosed during two years period, it was observed that among 145 (81%) dogs from the profile I, 82% were asymptomatic and 18% symptomatic ones; among 21 (11,7%) from the profile II, all (100%) were asymptomatic; and among 13 (7,3%) from the profile III, 84,6% were asymptomatic and 15,4 % symptomatic ones. Besides this, it was noted that the clinical conversion from asymptomatic to symptomatic status was principally recorded in dogs from the profile I (40,2%) than those from the profiles II (5,8%) and III (9%). By the other side, only 3,2% dogs from the profile I [IFAT(+)/DTH(-)] converted DTH(+) response, while 80% dogs from the profile II [IFAT(-)/DTH(+)] converted IFAT(+) response. At last, it was demonstrated that 100% of death by CVL occurred amongst dogs from the profile I, being 85,7% from the prevalence and 14,3% from the incidence. Taking together all these results, it seems reasonable that interaction between parasite and canine immune response is principally supported by immunologic profile clearly vulnerable, the profile I [IFAT(+)/DTH(-)], which does not offer any resistance to parasite, became the dog highly susceptible to infection
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Rahman, Bhuiyan Taufiqur. "Humoral and cellular immune responses to Helicobacter pylori in Bangladeshi children and adults that may be related to protection /." Götborg : Department of Microbiology and Immunology, Institute of Biomedicine at Sahlgrenska Academy, University of Gotheburg, 2010. http://hdl.handle.net/2077/21536.

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Moreira, Iramirton Figueirêdo. "Imunidade humoral e celular de crianças com desnutrição crônica semi-internas no centro de recuperação e educação nutricional, CRE Maceió/AL - 2008." Universidade Federal de Alagoas, 2009. http://repositorio.ufal.br/handle/riufal/643.

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The World Health Organization defines protein-energy malnutrition as a range of pathological conditions that appear by a deficient supply, transport or use of nutrients by the body s cells causing an essential amino acid deficiency in DNA and RNA synthesis, which can lead to a substantial immune system impairment. The focus of this research was to evaluate humoral and cellular immunity in children suffering from moderate to severe chronic malnutrition. The cross-sectional study was conducted with children 24-59 months old and 29 days, semi-interned at the Nutritional and Education Recovery Center (CREN), Maceió/AL, suffering from chronic malnutrition. At the same time creating a control group using normal similar aged children, randomly selected enrolled elementary school students from the same community. For data collection a standardized questionnaire was administered to children s parents and guardians addressing the history of infectious diseases. Cellular immunity assessment was performed by counting leukocytes and lymphocytes, B lymphocytes and T and delayed hypersensitivity test. Humoral immunity assessment was determined by immunoglobulins IgA, IgG and IgM in serum and IgG antibody by tetanus toxoid. Nutritional status was determined by the height-for-age (H/A) index. Data analysis used parametric and nonparametric statistics with a significance level (p<0.05). Research participants consisted of 68 children, 34 chronically malnourished and 34 well nourished. Among the malnourished 56% were male versus 47% normal weight, and the (H/A) index ranged from -4.61 to -2.02 in malnourished children versus -0.99 to 1.17 in eutrophic children. The history of airway infections, acute diarrhea, mumps and whooping cough was higher among the malnourished, but there was no statistical difference. The number of leukocytes and lymphocytes was significantly higher in malnourished children (p = 0.00). The number of B and T lymphocytes and delayed hypersensitivity test was not statistically different between the two groups. Serum immunoglobulins IgG and IgA were significantly (p = 0.00) higher among malnourished. Among the malnourished children an apparent decrease of 70.5% of IgG antibodies specific for tetanus toxoid versus 41.2% for normal weight (p = 0.01). Conclusion: There was no humoral and cellular immunity impairment in malnourished children but the number of T lymphocytes was lower and the production of IgG antibodies to tetanus toxoid was significantly lower in severely malnourished children.
A Organização Mundial da Saúde define Desnutrição Energético-Protéica como uma gama de condições patológicas que aparece por deficiência de aporte, transporte ou utilização de nutrientes pelas células do organismo provocando uma deficiência de aminoácidos essenciais na síntese de DNA e RNA, que pode levar a um considerável comprometimento do sistema imune. O objetivo do presente estudo foi avaliar a imunidade humoral e celular de crianças com desnutrição crônica moderada e grave. Estudo do tipo transversal realizado com crianças de 24 a 59 meses e 29 dias, semi-internas no Centro de Recuperação e Educação Nutricional, Maceió/AL, portadoras de desnutrição crônica. No mesmo período constituiu-se um grupo controle composto de crianças eutróficas da mesma faixa etária, selecionado aleatoriamente entre os alunos matriculados na escola de ensino fundamental da mesma comunidade. Para coleta de dados foi utilizado um questionário padronizado, aplicado aos pais ou responsáveis, abordando o histórico das crianças sobre doenças infecciosas. A avaliação da imunidade celular foi realizada através da contagem dos leucócitos e linfócitos totais, linfócitos B e T, e do teste de hipersensibilidade tardia. Para avaliar a imunidade humoral foi feita a determinação das imunoglobulinas IgA, IgG e IgM séricas, e anticorpo do tipo IgG para toxóide tetânico. O estado nutricional foi determinado pelo índice altura para idade (A/I). Na análise dos dados utilizou-se estatística paramétrica e não-paramétrica com nível de significância (p<0,05). Participaram do estudo 68 crianças, sendo 34 desnutridas crônicas e 34 eutróficas. Entre os desnutridos 56% eram do sexo masculino versus 47% dos eutróficos; o índice A/I variou de -4,61 a -2,02 nas crianças desnutridas versus -0,99 a 1,17 nas eutróficas. O histórico de infecções das vias aéreas, diarréia aguda, caxumba e coqueluche foi maior entre os desnutridos, porém não foi observada diferença estatística. O número de leucócitos e linfócitos totais foi significativamente maior nas crianças desnutridas (p = 0,00). O número de linfócitos B e T, e o teste de hipersensibilidade tardia não diferiu estatisticamente entre os dois grupos. As imunoglobulinas séricas IgA e IgG foram significativamente (p = 0,00) mais elevadas entre os desnutridos. Entre as crianças desnutridas 70,5% apresentaram diminuição de anticorpos específicos do tipo IgG para toxóide tetânico versus 41,2% das eutróficas (p = 0,01). Concluiu-se que não houve comprometimento da imunidade celular e humoral nas crianças desnutridas, porém é preciso ressaltar que o número de linfócitos T foi menor e a produção de anticorpos do tipo IgG para toxóide tetânico foi significativamente menor nas crianças desnutridas crônicas.
6

SILVA, Bárbara Brooklyn Timóteo Nascimento. "Aspectos imunológicos do caramujo Pomacea lineata (Spix, 1827) sob condições de estivação induzida." Universidade Federal Rural de Pernambuco, 2014. http://www.tede2.ufrpe.br:8080/tede2/handle/tede2/5039.

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Pomacea lineata (Spix, 1827) is a pulmonate gastropod that has a large dependence on humidity, Ampullaridae belongs to the family whose geographic distribution includes almost all the Neotropical Region , which inhabits waters of course slow and stagnate. Pulmonate gastropods have a conspicuous ecological feature, aestivation, which is a form of resistance and adaptation probably best defined as a survival strategy to cope with the arid conditions, but is also typically associated with lack of food availability, and often with high ambient temperatures. During these periods of aestivation some physiological aspects can be changed, as in molluscs, most of these is temperature dependent and can be altered by its variation, including the activity of the immune system. The innate immune system of invertebrates involves humoral and cellular response similar to that found in vertebrates. The cellular defenses occurs in combination with humoral defenses. Humoral responses include the production of reactive oxygen species (ROS) and nitric oxide (NO) and phenol oxidase enzyme activity, and cellular immune reactions are performed by hemocytes, performing, among other functions, encapsulation and phagocytosis of the pathogen. Thus, this research aimed to obtain information on some immunological parameters snail P. lineata in conditions of induced aestivation. The snails were induced to aestivation through the gradual withdrawal of water in the aquarium and abstention from food, getting in these conditions for 60 days. After this period, hemolymph of 40 individuals were collected for analysis of the total haemocyte count, measurement of nitric oxide, phenol oxidase activity and total protein. The results revealed that animals under aestivation showed a significant increase in the total number of hemocytes and measurement of nitric oxide, which may confer greater chance of survival.
Pomacea lineata (Spix, 1827) é um gastrópode pulmonado que apresenta uma grande dependência da umidade, pertencente à família Ampullaridae cuja distribuição geográfica inclui quase toda a Região Neotropical, na qual habita águas de curso lento e estagnadas. Gastrópodes pulmonados apresentam uma característica ecológica conspícua, a estivação, que é uma forma de resistência e adaptação provavelmente melhor definida como uma estratégia de sobrevivência para lidar com as condições áridas, mas também é tipicamente associada com a falta de disponibilidade de alimentos e, frequentemente, com as altas temperaturas ambientais. Durante estes períodos de estivação alguns aspectos fisiológicos podem ser alterados, pois nos moluscos, a maioria desses, é dependente da temperatura e podem ser alterados pela sua variação, incluindo a atividade do sistema imunitário. O sistema imunológico inato dos invertebrados envolve a resposta celular e humoral similarmente ao encontrado nos vertebrados. As defesas celulares ocorrem em combinação com as defesas humorais. As respostas humorais, incluem a produção de espécies reativas de oxigênio (ROS) e óxido nítrico (NO) e a atividade da enzima fenoloxidase, e as reações imunes celulares são realizadas pelos hemócitos, que executam, dentre outras funções, o encapsulamento e fagocitose do patógeno. Assim, esta pesquisa teve por objetivo obter informações sobre alguns parâmetros imunológicos do caramujo P. lineata em condições de estivação induzida. Os caramujos foram induzidos à estivação através da retirada gradual de água no aquário e abstenção de alimento, ficando nestas condições por 60 dias. Após este período, hemolinfa de 40 indivíduos foram coletadas para as análises de contagem total de hemócitos, dosagem de óxido nítrico, atividade da fenoloxidase e proteínas totais. Os resultados revelaram que os animais estivantes apresentavam um aumento significativo no número total de hemócitos e na dosagem de óxido nítrico, o que pode conferir maior chance de sobrevivência.
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Hein, Héber Eduardo. "Influência da imunidade de matrizes suínas na resposta à vacinação de leitões contra Mycoplasma hyopneumoniae." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2015. http://hdl.handle.net/10183/127074.

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A suinocultura está amplamente difundida no Brasil, o quarto maior produtor mundial de carne suína. Seu efetivo está concentrado em maior parte na região Sul, com 48,8% dos suínos. Porém, a intensificação e o confinamento das criações expõem os animais a agentes patogênicos, como o Mycoplasma hyopneumoniae (Mhyo), causador da Pneumonia Enzoótica Suína (PES). A doença é caracterizada pela ocorrência de tosse seca não produtiva e lesões pulmonares de consolidação, denominadas hepatização. A vacinação de leitões é uma importante ferramenta empregada no controle da PES. Contudo, é relatado que a imunidade passiva adquirida pelos leitões através do colostro das matrizes suínas pode interferir na sua resposta à vacinação contra o Mhyo. Desta forma, este trabalho teve como objetivo avaliar a influência da imunidade materna na resposta à imunização de leitões contra Mhyo ao desmame. Dez matrizes foram divididas em dois grupos baseado na Razão S/P de um teste ELISA comercial , um com baixo nível de anticorpos (Ac) anti-Mhyo (BAc, Razão S/P <0,75) e outro com alto nível (AAc, Razão S/P ≥0,75). De cada fêmea, dois leitões eram controles (contr) e nove vacinados (vac) contra Mhyo. Estes grupos e tratamentos foram comparados entre si quanto a parâmetros de imunidade humoral, celular e comprometimento pulmonar ao abate. Após a ingestão de colostro, os leitões das fêmeas AAc mantiveram os maiores níveis de Ac, até os 56 dias de idade. Quando avaliados através do teste ELISA, dos 13 aos 99 dias depois de vacinados os leitões BAc-vac apresentaram níveis de Ac mais estáveis, com um aumento significativo aos 113 dias pós-vacinação. Os parâmetros celulares não diferiram entre grupos e tratamentos, com exceção dos linfócitos T CD4+CD8+, com menores percentuais entre os vacinados. Independente do grupo, os vacinados tiveram menor comprometimento pulmonar, porém os BAc-vac tiveram menos lesões que os AAc-vac. Os resultados demonstraram que a vacinação dos leitões contra Mhyo ao desmame os protege contra o agente, levando ao menor comprometimento pulmonar, principalmente quando a imunização ocorre na presença de baixos níveis de Ac passivos.
Swine production is widespread in Brazil, being the fourth largest producer of pork meat. Swinesare concentrated in the Southern region, comprising 48.8%of pig population. However, due to confinement system, pigs are exposed to pathogens such as the bacteria Mycoplasma hyopneumoniae (Mhyo), responsible for swine enzootic pneumonia (SEP). The disease is characterized by a dry, nonproductive cough, and macroscopic areas of consolidation in the lung. The piglet vaccination is an important practice to SEP control. However, it is reported that passive immunity acquired by the piglets through the colostrum of sows may affect their response to vaccination against Mhyo. The objective of this study was to evaluate the influence of maternal immunity in the pig vaccination against Mhyo after weaning. Ten sows were divide in two groups according with the ELISA’s S/P Ratio, with low (LAb, S/P Ratio <0.75) or high (HAb, S/P Ratio ≥0.75) level of antibodies (Ab). From each sow, two piglets were controls (contr) and nine vaccinated (vac) against Mhyo. Piglets' humoral and cellular immunity and pulmonary lesions were compared between the treatments and groups of sows.The Ab level after colostrum intake was higher in piglets from HAb group of sows until 56 days of age. When evaluated by ELISA, LAb-vac piglets showed a more stable Ab levels from 13 to 99 days post-vaccination, with a significant increase at 113 days post-vaccination. No differences were detected between groups and treatments according with cellular parameters, except T CD4+CD8+ lymphocytes percentages, that were lower in vaccinated piglets. Regardless of the group, vaccinated pigs had lower pulmonary lesions, but the LAb-vac piglets had less damage than the HAb-vac. These results demonstrated that piglet vaccination against Mhyo at weaning protects them against the pathogen and provides lower pulmonary lesions, especially when the immunization occurs in the presence of low levels of maternal Ab.
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Beattie, Lynette. "The role of the spleen in Malaria : Cellular changes that affect the development of immunity." Queensland University of Technology, 2006. http://eprints.qut.edu.au/16195/.

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Malaria, caused by the apicomplexan parasite Plasmodium, is a major cause of morbidity and mortality throughout the world. This study has focused on the role of the spleen in the control of the blood stage of infection. Three aspects have been examined specifically: the effect of infection on the architecture of the spleen, the role of the spleen in parasite clearance and the formation of B cell memory. Firstly, the effect of infection on the splenic microarchitecture was examined. An essential component of the splenic architecture is the marginal zone (MZ), an area of the spleen that separates the reticuloendothelial red pulp of the spleen from the lymphoid white pulp compartment. Two unique populations of macrophages are found in the marginal zone: marginal zone macrophages (MZM) and marginal metallophilic macrophages (MMM). In the current study, parasitised red blood cells (pRBC) as well as normal RBC located to the MZ thirty minutes after intravenous injection and formed close associations with both MMM and MZM. Eight days after infection, at the time of peak parasitemia, a complete loss of both MMM and MZM was observed. Assays to detect cell death revealed that the loss of both MMM and MZM appeared to occur as a result of apoptosis. The apoptosis was not induced by up regulation of the inflammatory cytokines tumour necrosis factor or interferon-γ and could not be blocked by over expression of the apoptosis inhibitor Bcl2. Significantly, MMM were retained in the absence of CD8+ T cells implicating CD8+ T cells in the loss of MMM. Finally, infection of CD95-/- mice demonstrated that CD95/CD95-ligand (Fas/Fas-ligand) interactions were responsible for some of the CD8+ T cell-mediated loss of MMM. These data provide evidence for a novel interaction between MMM and CD8+ T cellsfollowing infection with Plasmodium. Secondly, the role of the spleen in the control of parasitemia and disease was monitored with an emphasis on determining the role of splenic macrophage populations (MMM, MZM and red pulp macrophages [RPM]) in parasite clearance. A clodronate liposome-mediated macrophage depletion technique was used, and caused a complete loss of all three macrophage sub-populations, as well as 50% of splenic dendritic cells, within 24 hours of administration. Each of the macrophage populations, as well as splenic DC, demonstrated different repopulation kinetics following their depletion from the spleen and these kinetics were utilised to examine each cell population in isolation. RPM depleted mice had significantly higher peak parasitemias than the controls. This peak returned to the level observed in undepleted control animals only after the repopulation of RPM was complete, suggesting that RPM play a role in the control of peak parasitemia following infection. Neither MMM nor MZM played a role in the control of parasitemia. The role of non-splenic macrophages and splenic dendritic cells also was investigated and shown to be insignificant in the absence of splenic macrophages. Finally, the role of RPM in mice immune to infection was investigated and their role shown to be dispensable, with immune mice clearing parasitemia efficiently in the absence of RPM. RPM therefore are important for the innate control of infection with P. chabaudi but are dispensible once adaptive immunity is established. Finally, the role of the spleen in the development of parasite-specific B cell memory was examined. Initial studies demonstrated that germinal centre (GC) development was compromised following infection with P. chabaudi, with an involution of B cell follicles noted early in infection. Adoptive transfer of memory B cells from immunised to naïve mice demonstrated that some protection was conferred on recipient mice by parasite-specific memory B cells. But, the memory B cells could not protect the host from developing parasitemia and did not produce significant amounts of parasite-specific immunoglobulin within seven days of challenge infection. Memory B cells could not be detected ten weeks after infection, indicating that the development, or survival, of parasite-specific memory B cells was compromised. The development of bystander memory B cells was not affected by infection. Finally, long-lived plasma cells were shown to develop in response to infection, although re-exposure of the cells to parasites in the form of recrudescent parasitemia resulted in their loss. This study therefore has identified a defect in the development of long-term, B cell-mediated, protection against infection with P. chabaudi. Each of these factors has significant implications for the understanding of how the spleen contributes to the control of infection with Plasmodium and potential applications for the further development of malaria vaccines and treatment regimens.
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Silva, Milton Thiago Guerino da. "Avaliação de potencial agente vacinal contra o S.pyogenes em camundongos transgênicos, portadores de genes HLA de classe II humanos." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/5/5146/tde-20122011-155537/.

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A faringite estreptocócica desencadeada pelo Streptococcus pyogenes pode resultar em uma série de doenças humanas e complicações como a febre reumática (FR) em indivíduos predispostos não tratados. A FR é uma doença autoimune que afeta mais de 20 milhões de crianças em países em desenvolvimento. A proteína M presente na membrana do S. pyogenes representa o maior fator de virulência da bactéria, e é objetivo de estudos para o desenvolvimento de uma vacina contra essa patologia. Atualmente mais de 200 tipos de proteínas M foram descritos na literatura e a sua porção Cterminal é conservada entre os diferentes tipos. Desenvolvemos um protótipo de vacina que compreende 55 resíduos de aminoácido da porção C-terminal, denominado StreptInCor. Neste trabalho analisamos a resposta humoral e celular específica contra o peptídeo sintético StreptInCor, usando camundongos transgênicos portadores de HLA de classe II humanos DR2, DR4, DQ6 e DQ8. O protocolo de imunização consistiu em administrar 50 g do StreptInCor adsorvido em 300 g de hidróxido de alumínio nos dias 0 e 14. Os grupos controles foram injetados com salina nas mesmas condições. O soro obtido no 28º dia foi testado por ensaio imunoenzimático (ELISA) para verificarmos a presença de anticorpos contra o StreptInCor e os esplenócitos destes animais, obtidos nessa data, foram utilizados para ensaios de proliferação celular na presença do StreptInCor. Testes de segurança foram efetuados e não observamos reação cruzada contra a miosina cardíaca e após 12 meses de acompanhamento, amostras de tecidos desses animais foram submetidas à análise histológica. Em conclusão não verificamos indícios de reações autoimunes nos animais imunizados com o StreptInCor e os resultados obtidos mostram a capacidade do StreptInCor em desencadear uma resposta imune, duradoura e segura em camundongos portadores de moléculas HLA de classe II
Streptococcal pharyngitis triggered by Streptococcus pyogenes throat infection can result in rheumatic fever (RF) and rheumatic heart disease (RHD) in untreated susceptible individuals. RF is an autoimmune disease that affects more than 20 million children in developing countries. M protein is the major factor of virulence of the bacteria, and it has been studied to develop a vaccine. Currently more than 200 M protein types have been described and its Cterminal domain is conserved in many different serotypes. We developed a vaccine epitope (StreptInCor) composed by 55 amino acid residues of the Cterminal portion of the M protein. In the present work we analyze the ability of the StreptInCor of induce immune response in HLA class II transgenic mice. The transgenic mice harboring the HLA Class II DR2, DR4, DQ6 and DQ8 were immunized subcutaneously with 50 g StreptInCor adsorbed onto 300 g of aluminum hydroxide gel on days 0 and 14. Control groups were immunized with vehicle (Saline) in same conditions. The sera were obtained on day 28 and tested by ELISA to verify the presence of antibodies. The specific cellular immune response was evaluated by proliferation assay using splenocytes. No cross reaction with cardiac myosin were observed. Tissue samples from immunized mice followed by 12 months were analyzed in order to verify if StreptInCor induces some histological damage. No autoimmune or deleterious reactions were observed. In conclusion our results indicate that StreptInCor Induces a good and prolonged and safe immune response in HLA class II transgenic mice
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Shidani, Babak. "Effet de la cyclosporine a sur le systeme immunitaire de la souris." Paris 7, 1987. http://www.theses.fr/1987PA077159.

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Книги з теми "Humoral and cellular immunity":

1

Federation of Immunological Societies of Asia-Oceania. Congress. 2nd Congress of the Federation of Immunological Societies of Asia-Oceania: Bangkok, Thailand, January 23-27, 2000. Edited by Sirisinha Stitaya, Chaiyaroj Sansanee C, and Tapchaisri Pramuan. Bologna, Italy: Monduzzi Editore, International Proceedings Division, 2000.

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2

Goss, John A. The thymus: Regulator of cellular immunity. Austin: R.G. Landes Co., 1993.

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3

Hašek, Milan. Buněčné a molekulární základy specifické imunity. Praha: Academia, 1988.

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4

Austyn, Jonathan M. Principles of cellular and molecular immunology. Oxford: Oxford University Press, 1993.

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5

International, Symposium on Cellular Immunotherapy of Cancer (1986 Racine Wis ). Cellular immunotherapy of cancer: Proceedings of the International Symposium on Cellular Immunotherapy of Cancer, held at Racine, Wisconsin, October 30-November 1, 1986. New York: Liss, 1987.

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6

International Symposium on Cellular Immunotherapy of Cancer (1986 Racine, Wis.). Cellular immunotherapy of cancer: Proceedings of the International Symposium on Cellular Immunotherapy of Cancer, held at Racine, Wisconsin, October 30-November 1, 1986. Edited by Truitt Robert L. ed, Gale Robert Peter ed, and Bortin Mortimer M. ed. New York: Liss, 1987.

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7

International, Symposium on Cellular Immunotherapy of Cancer (1986 Racine Wis ). Cellular immunotherapy of cancer: Proceedings of the International Symposium on Cellular Immunotherapy of Cancer, held at Racine, Wisconsin, Oct. 30 - Nov. 1, 1986. New York: Liss, 1987.

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8

Abbas, Abul K. Cellular and molecular immunology. 7th ed. Philadelphia: Elsevier/Saunders, 2012.

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9

NATO Advanced Research Workshop on Cellular and Humoral Immunological Components of Cerebrospinal Fluid in Multiple Sclerosis (1986 Engelhoef, Belgium). Cellular and humoral immunological components of cerebrospinal fluid in multiple sclerosis. New York: Plenum Press, 1987.

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10

Lowenthal, A., and J. Raus, eds. Cellular and Humoral Immunological Components of Cerebrospinal Fluid in Multiple Sclerosis. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4899-5348-3.

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Частини книг з теми "Humoral and cellular immunity":

1

Nauta, Jozef. "Humoral and Cellular Immunity." In Statistics in Clinical Vaccine Trials, 13–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-14691-6_2.

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2

Nauta, Jozef. "Humoral and Cellular Immunity." In Springer Series in Pharmaceutical Statistics, 15–19. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-37693-2_2.

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3

Heyman, Birgitta. "Antibody Mediated Regulation of Humoral Immunity." In Molecular and Cellular Mechanisms of Antibody Activity, 221–49. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7107-3_9.

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4

Virgin, H. W., T. S. Dermody, and K. L. Tyler. "Cellular and Humoral Immunity to Reovirus Infection." In Current Topics in Microbiology and Immunology, 147–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-72095-6_8.

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5

Gorer, P. A. "Interactions Between Sessile and Humoral Antibodies in Homograft Reactions." In Ciba Foundation Symposium - Cellular Aspects of Immunity, 330–47. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470719169.ch16.

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6

Ulcová-Gallová, Zdenka, and D. Sedlácek. "Cellular and Humoral Immunity to Sperm in Ovulatory Cervical Mucus from Infertile Women." In Advances in Experimental Medicine and Biology, 395–97. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1941-6_82.

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7

Bottomly, Kim. "Immunosemiotics: Whither the Immune Response? Factors Directing the Response to Humoral or Cell-Mediated Immunity." In The Semiotics of Cellular Communication in the Immune System, 305–8. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73145-7_27.

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8

Bachraoui, Moussa, Khalid Hattaf, and Noura Yousfi. "Spatiotemporal Dynamics of Fractional Hepatitis B Virus Infection Model with Humoral and Cellular Immunity." In Trends in Biomathematics: Chaos and Control in Epidemics, Ecosystems, and Cells, 293–313. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-73241-7_19.

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Mantovani, Alberto, Barbara Bottazzi, Andrea Doni, Giovanni Salvatori, Pascale Jeannin, and Cecilia Garlanda. "Phagocytes Are a Source of the Fluid-Phase Pattern Recognition Receptor PTX3: Interplay between Cellular and Humoral Innate Immunity." In Phagocyte-Pathogen Interactions, 171—P2. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555816650.ch10.

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Gooch, Jan W. "Humoral Immunity." In Encyclopedic Dictionary of Polymers, 899. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13953.

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Тези доповідей конференцій з теми "Humoral and cellular immunity":

1

Orlenkovich, Lilija. "CORRELATIONS ANALYSIS OF IMMUNE SYSTEM AND GUT MICROBIOTA INDICES OF RATS IN THE CHRONIC EXPOSITION TO BIOINSECTICIDE ENTOMOPHTHORIN." In XIV International Scientific Conference "System Analysis in Medicine". Far Eastern Scientific Center of Physiology and Pathology of Respiration, 2020. http://dx.doi.org/10.12737/conferencearticle_5fd728a1ea3837.21988844.

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Анотація:
The analysis of the variation in the number, intensity and direction of correlations between the immune system and the gut microbiota of rats revealed that the T-, B-system and humoral immunity changes as well as cellular and humoral factors of an organism nonspecific defense are accompanied by changes of the Intestinal microbiota of intact and experimental rats
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Zavadova, Eva, Bohuslav Konopasek, Michal Vocka, Michaela Miskovicova, Jan Spacek, Terezie Fucikova, and Lubos Petruzelka. "Abstract B9: Abnormalities in cellular and humoral immunity in breast cancer patients resistant to endocrine therapy." In Abstracts: AACR Special Conference on Tumor Immunology: Multidisciplinary Science Driving Basic and Clinical Advances; December 2-5, 2012; Miami, FL. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tumimm2012-b9.

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Rondaan, C., K. van der Geest, E. Eelsing, N. Bos, J. Westra, and E. Brouwer. "FRI0317 Humoral and cellular immunity to varicella-zoster virus in giant cell arteritis patients: no evidence of viral reactivation at onset of disease." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.3756.

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Tian, Yuling, and Peng Ren. "A Clustering Model Inspired by Humoral Immunity." In 2009 International Workshop on Intelligent Systems and Applications. IEEE, 2009. http://dx.doi.org/10.1109/iwisa.2009.5072611.

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Michel, Kristin. "The regulation of humoral control immunity in mosquitoes." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.92697.

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Hentley, William Thomas. "Bedbug cellular immunity." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.109396.

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Pradeep, B. G. Sampath Aruna, and Hazrat Ali. "Global stability properties for a delayed virus dynamics model with humoral immunity response and absorption effect." In 2017 International Conference on Electrical Engineering (ICEE). IEEE, 2017. http://dx.doi.org/10.1109/icee.2017.7893424.

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Zborovsky, AB, IP Gontar, AV Alexandrov, LA Maslakova, GF Sychova, and OI Emelyanova. "AB0105 Dynamics of humoral immunity indices in systemic sclerosis patients depending on the therapy carried out." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.253.

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Хотулева, А. Г. "Features of changes in the parameters of humoral immunity in occupational asthma in combination with metabolic syndrome." In The second international youth Forum "OCCUPATION AND HEALTH". PT "ARIAL", 2018. http://dx.doi.org/10.31089/978-5-907032-51-4-2018-1-277-281.

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Dammermann, W., K. Bröker, S. Pischke, C. Vinnemeyer, and S. Lüth. "Anti-HEV humoral immunity in long term travellers from Germany to tropical regions in Asia and Africa." In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677252.

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Звіти організацій з теми "Humoral and cellular immunity":

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Rusanova, O. A., I. P. Gontar, O. A. Emelyanova, L. A. Maslakova, and Yi A. Trubenko. MANIFESTATIONS OF HUMORAL IMMUNITY TO FIBRONECTIN AS PART OF CLINICAL PRESENTATIONS OF RHEUMATOID ARTHRITIS. Планета, 2018. http://dx.doi.org/10.18411/978-5-907109-24-7-2018-xxxiv-97-99.

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Middlebrooks, Bobby L. Investigation of the Role of Immunoglobulin Classes and Subclasses in Humoral and Mucosal Immunity in Cetaceans. Fort Belvoir, VA: Defense Technical Information Center, June 2005. http://dx.doi.org/10.21236/ada452454.

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Gontar, I. P., O. A. Rusanova, A. S. Trofimenko, O. I. Emelyanova, L. A. Maslakova, and N. Emelyanov. CARDIOVASCULAR CONDITIONS IN PATIENTS WITH SYSTEMIC SCLERODERMA THAT ARE ASSOCIATED WITH HUMORAL IMMUNITY IMPAIRMENT TO ELASTIN AND ELSTASE. Планета, 2018. http://dx.doi.org/10.18411/978-5-907109-24-7-2018-xxxiv-54-55.

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Hrushesky, William J. Preliminary Investigation of the Role of Cellular Immunity in Estrous Cycle Modulation of Post-Resection Breast Cancer Spread. Fort Belvoir, VA: Defense Technical Information Center, December 2002. http://dx.doi.org/10.21236/ada415581.

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Hrushesky, William J. Preliminary Investigation of the Role of Cellular Immunity in Estrous Cycle Modulation of Post-Resection Breast Cancer Spread. Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada421466.

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Hrushesky, William J. Preliminary Investigation of the Role of Cellular Immunity in Estrous Cycle Modulation of Post-Resection Breast Cancer Spread. Fort Belvoir, VA: Defense Technical Information Center, May 1999. http://dx.doi.org/10.21236/ada392521.

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