PROTEIN MALNUTRITION & HELPER T CELL SUPPORT OF SIGA

拟议研究的主要目标是确定 分泌型免疫球蛋白（sIg）A受损的病因学 在膳食蛋白质缺乏期间观察到的生产。 这 损伤可能有助于增强微生物感染 或在蛋白质降解过程中口腔和粘膜表面的定植 营养不良 总IgA和抗原特异性分泌型（S）伊加 （经口攻毒后， 唾液和肠分泌物中的变形菌，使用酶 免疫测定（ETA）将在喂食20%（20 C）或4%的小鼠中确定 (4C)酪蛋白饮食形成断奶。 sIgA降低的意义 将通过评估口语或 肠道病原体在相应的表面上定殖。 的 假设饮食蛋白减少伊加改变 与辅助相关的特异性T细胞亚群（H）（L3T4+）或 抑制（S）（Lyt 2+），伊加免疫应答将被 测试. T细胞的组织学鉴定和定量 切除的唾液腺、派伊尔集合淋巴结和脾脏中的亚群 在感染前后喂食4 ℃或20 ℃的小鼠将需要 使用L3 T4或Lyt 2抗体的免疫荧光。 使用 相同的抗体，每个子集将从分散的 通过“淘选”产生免疫球蛋白A增强的能力， 将在感染前和感染过程中评估这些因素。 L3T4+ T 细胞伊加增强性淋巴因子包括白细胞介素5（IL 5），IL 4， IL 2。 将检测多克隆刺激的T细胞上清液 使用EIA促进伊加产生的能力，而不是 IgG、IgG1和IgM，由纯化的B细胞刺激产生 脂多糖（LPS）。 由于HT可产生IL 4、IL 5， 细胞亚群不同于产生IL 2的HT细胞亚群， 将使用以下方法估计这些组织中每个子集的频率 有限稀释分析 注意到IgA增强淋巴因子 在喂食4C的小鼠中受损，将尝试 通过治疗重建喂食4C的小鼠中的分泌型伊加水平 用合适的重组淋巴因子。 这项研究将 有助于了解口腔健康的问题， 营养不良的人口，因为他们与减少 分泌免疫和口腔健康。

The major objective of the proposed research is to determine the etiology of the impaired secretory immunoglobulin (sIg) A production observed during dietary protein deficiency. This impairment likely contributes to the enhanced microbial infection or colonization of oral and mucosal surfaces during protein malnutrition. Total and antigen-specific secretory (S) IgA (following oral challenge with Giardia muris or Streptococcus mutans in saliva and intestinal secretions, using enzyme immunoassay (ETA), will be determine in mice fed 20% (20C) or 4% (4C) casein diets form weaning. The significance of sIgA reduction will be demonstrated by evaluating the ability of oral or intestinal pathogens to colonize at the respective surfaces. The hypthesis that dietary protein reductions reduces IgA by altering specific T cell subsets associated with help (H) (L3T4+) or suppression (S) (Lyt 2+), of the IgA immune response will be tested. Histological identification and quantification of T cell subsets in excised salivary glands, Peyer's patches, and spleen of mice fed 4C or 20C before and after infection will entail immunofluorescence using antibodies to L3T4 or Lyt2. Using the same antibodies, each subset will be isolated from dispersed tissues by "panning"; and the ability to generate IgA-enhancing factors will be evaluated before and during infection. L3T4+ T cell IgA enhancing lymphokines included, Interleukin 5 (IL5), IL4, IL2. Polyclonally stimulated T cell supernatants will be tested using EIA for the ability to promote IgA production, as opposed to IgG, IgG1 and IgM, production from purified B cells stimulated with lipopolysaccharide (LPS). Since IL4, IL5 could be generated by HT cell subsets distinct from IL2-generating HT cell subsets, the frequency of each subset in these tissues will be estimated using limiting dilution analysis. Noting the IgA-enhancing lymphokine which is impaired in mice fed 4C, attempts will be made to reconstitute the secretory IgA levels in mice fed 4C by treatment with the appropiate recombinant lymphokine. This research will contribute to understanding the problems of oral health in malnourished human populations as they relate to decreased secretory immunity and oral health.