Orientador: Paulo Inácio da Costa / Banca: Virginia Paes Leme Ferriani / Banca: Cleni Mara Marzocchi Machado / Resumo: A alergia à proteína do leite de vaca (APLV) é comum no primeiro ano de vida e o seu reconhecimento e diagnóstico são difíceis. A proposta deste estudo é verificar a expressão de fenótipos linfocitários, as citocinas padrão Th1 e Th2, e a IgE total e específica em crianças com APLV, crianças atópicas (AC) e não atópicas (NAC) e suas respectivas mães.Foram colhidas amostras de sangue periférico para tipagem de linfócitos por citometria de fluxo, e dosadas as citocinas séricas, por CBA (Cytometric Bead Array) e dosado a IgE total e específica para as proteínas caseína, α lactoalbumina e β lactoglobulina , das crianças e suas mães nos grupos APLV, AC e NAC.Nas crianças do grupo APLV o início dos sintomas foi por volta dos 5,1 meses de idade, com idade média de 17,25 meses (sd=14,8 meses). As crianças e suas mães dos grupos alérgicos (APLV e AC) mostraram maior número de linfócitos CD4+CD25+ (p<0,05) em relação àquelas do grupo não alérgico (NAC), mas sem diferença significativa (p>0,05) entre os grupos APLV e AC. O grupo APLV mostrou maior tendência à presença do fenótipo CD25. As concentrações séricas das citocinas IL4, IL5, IL10, IL2, TNF-α e IFN-γ, entre os grupos estudados, não apresentaram diferenças estatísticas significantes (p>0,05), porém houve uma maior tendência à expressão da IL10 nas crianças do grupo APLV. A IgE total ficou mais evidente no grupo APLV do que nos demais grupos, e os principais alérgenos foram a α-lactoalbumina e β lactoglobulina. As crianças com alergia ao leite de vaca apresentam uma maior positividade de linfócitos CD4+CD25+, presença de IgE total e expressão de IL10 in vivo o que também pode sugerir um meio de controle da alergia para desenvolver tolerância à proteína do leite de vaca... (Resumo completo, clicar acesso eletrônico abaixo) / Abstract: The allergy to cow‟s milk protein (CMA) is common in the first year of life and it is difficult to acknowledge and diagnose it. This study aims to verify the expression of lymphocyte phenotypes, detect the TH2 and TH1 pattern cytokines and the total and specific IgE in CMA children, in atopic (AC) and non-atopic (NAC) children and their respective mothers. Samples of peripheral blood were collected in order to type the lymphocytes by flow cytometry, dosed the serial cytokines by Cytometric Bead Array (CBA) and dosed the total IgE and specific IgE for the casein, α lactoalbumin and β lactoglobulin proteins of the children and their mothers in the CMA, AC and NAC groups. In the CMA children the symptoms first occurred around 5,1months old, with the average age of 17.25 months (sd=14.8 months). The children and their mothers from the allergic group (CMA and AC) showed significantly presence of CD4+CD25+ lymphocytes (p<0.05) higher than the non-allergic group (NAC), but without any significant difference (p>0.05) between the CMA and AC groups, although there was a tendency to an increase presence of these cells in the CMA group. The serial concentration of the IL4, IL5, IL10, IL2, TNF-α and IFN-γ cytokines, among the studied groups, did not present significant statistical difference (p>0.05), however, there was a tendency to an increase expression of IL10 in the CMA group of children. The total IgE was more evident in the CMA group than in the other ones and the main proteins which caused allergic reactions were α-lactoalbumin e β lactoglobulin. The children with cow‟s milk allergy presented a higher positivity of CD4+CD25+ lymphocytes, higher total IgE and an increase expression of in vivo IL10, which may also suggest a means of control of the allergy to develop tolerance to the cow‟s milk proteins... (Complete abstract click electronic access below) / Mestre

Thesis (M.A.) -- University of Texas at Arlington, 2008.

No description available.

No description available.

Thesis (M.S.P.H.)--University of Michigan, 1941.

Thesis (M.S.P.H.)--University of Michigan, 1941.

Thesis (Ph.D.)--University of Nebraska-Lincoln, 2008. / Title from title screen (site viewed Mar. 5, 2009). PDF text: xiv, 231 p. : ill. (some col.) ; 4.69 Mb. UMI publication number: AAT 3331368. Includes bibliographical references. Also available in microfilm and microfiche formats.

Thesis (M.S.C.I.T.)--Regis University, Denver, Colo., 2005. / Title from PDF title page (viewed on Nov. 10, 2005). Includes bibliographical references.

Thesis (M.A.) -- Central Connecticut State University, 2006. / Thesis advisor: Marc Goldstein. "... in partial fulfillment of the requirements for the degree of Master of Arts in Psychology." Includes bibliographical references (leaves 42-45). Also available via the World Wide Web.

Food allergy is a potentially life-threatening disease affecting up to 10% of individuals in Western countries. Clinical reactivity to food allergens is primarily mediated by immunoglobulin (Ig) E, with symptoms ranging from mild urticaria to anaphylaxis. Currently, food allergy remains a disease without a cure. Oral immunotherapy (OIT), which involves consuming small amounts of allergen, remains an experimental treatment in Canada, although has been approved by the Food and Drug Administration (FDA) in the United States for treatment of peanut allergy. While efficacious to induce desensitization, OIT is accompanied by a significant rate of adverse effects. Sublingual immunotherapy (SLIT) is a novel route of treatment for food allergy, where small amounts of allergen are placed under the tongue and held for 2-3 minutes. In contrast to OIT, SLIT offers not only treatment efficacy but also promises an excellent safety profile. The first objective of this thesis was to first develop a SLIT regimen in murine models of food allergy where sensitization is carried out either epicutaneously or intragastrically. Secondly, we investigated the efficacy of SLIT in modulating the clinical and humoral responses in prophylactic and semi-therapeutic settings. In the prophylactic setting, where SLIT was administered prior to sensitizing allergen exposures, SLIT-treated mice were completely protected from allergic sensitization including absent production of serum ovalbumin-specific IgE. In the semi-therapeutic setting, where SLIT was administered to mice primed to develop food allergy, it produced a partial protection against food-induced clinical reactivity. This was associated with lower levels of IgE production in comparison to non-treated, allergic mice. Together, this work provides both an optimized SLIT protocol, as well as evidence on the efficacy of SLIT in the treatment of food allergy in murine models. These findings will aid future work investigating the cellular and molecular mechanisms underlying SLIT-induced protection. / Thesis / Master of Science (MSc) / Food allergy is a potentially life-threatening disease which is primarily mediated by IgE antibodies. Strict allergen avoidance and use of rescue epinephrine upon accidental allergen exposure remain the standard of care. Oral immunotherapy, where individuals ingest small amounts of allergen, is currently the experimental treatment of reference to induce clinical tolerance; however, it is accompanied by a significant rate of adverse reactions. In contrast, sublingual immunotherapy (SLIT), which is less efficacious, upholds a superior safety profile. The primary objective of this thesis was to investigate the impact of SLIT in inducing clinical and immunological changes in murine models of food allergy. We demonstrated that when administered prophylactically, SLIT prevents mice from undergoing anaphylaxis. When administered to sensitized mice in a pre-allergic state, SLIT was protective against severe clinical reactivity after challenge. In conclusion, the work presented here establishes a useful platform to investigate the mechanisms underlying SLIT-mediated protection.