The IgE antibody system: mature, peripheral B lymphocytes exert regulatory influences on the IgE systems of self-reconstituting, sublethally irradiated mice.
{"title":"The IgE antibody system: mature, peripheral B lymphocytes exert regulatory influences on the IgE systems of self-reconstituting, sublethally irradiated mice.","authors":"D H Katz, C A Bogowitz, L R Katz","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Previous studies have documented clear biological differences, such as sensitivity to moderate doses of irradiation, between B lymphocytes of the IgE type and B lymphocytes of other immunoglobulin isotypes. The present experiments were originally designed to explore such differences further by comparing the abilities of B lymphocytes derived from various IgE responder phenotypes, which differ among various inbred mouse strains, to reconstitute in a positive way the ability of sublethally irradiated recipient mice (of syngeneic or semisyngeneic type) to mount specific immune responses of the IgE antibody class. This was an important question with regard to delineating fully underlying differences in IgE responder phenotypes among different mouse strains, since heretofore most of the emphasis in experimentally defining such differences has focused on differences in T cell function, rather than B cell function. The experimental approach chosen to address this question seemed logical for two reasons: 1) it was our expectation that following exposure to the dose of irradiation employed (700 rads), individual mice would only slowly repopulate peripheral lymphoid tissues with their own stem cell products, and hence the expression of IgE responsiveness observed could be expected to reflect the responsiveness of the donor B cell population transferred into such recipients; and 2) since recipient mice were carrier-primed one week prior to irradiation in order to create a pool of radioresistant carrier-specific helper T cells, one could expect that this amplified pool of helper T cells would hasten the development of antibody production by the transferred donor B cells.</p>","PeriodicalId":77639,"journal":{"name":"The Journal of molecular and cellular immunology : JMCI","volume":"1 2","pages":"83-9"},"PeriodicalIF":0.0000,"publicationDate":"1984-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Journal of molecular and cellular immunology : JMCI","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Previous studies have documented clear biological differences, such as sensitivity to moderate doses of irradiation, between B lymphocytes of the IgE type and B lymphocytes of other immunoglobulin isotypes. The present experiments were originally designed to explore such differences further by comparing the abilities of B lymphocytes derived from various IgE responder phenotypes, which differ among various inbred mouse strains, to reconstitute in a positive way the ability of sublethally irradiated recipient mice (of syngeneic or semisyngeneic type) to mount specific immune responses of the IgE antibody class. This was an important question with regard to delineating fully underlying differences in IgE responder phenotypes among different mouse strains, since heretofore most of the emphasis in experimentally defining such differences has focused on differences in T cell function, rather than B cell function. The experimental approach chosen to address this question seemed logical for two reasons: 1) it was our expectation that following exposure to the dose of irradiation employed (700 rads), individual mice would only slowly repopulate peripheral lymphoid tissues with their own stem cell products, and hence the expression of IgE responsiveness observed could be expected to reflect the responsiveness of the donor B cell population transferred into such recipients; and 2) since recipient mice were carrier-primed one week prior to irradiation in order to create a pool of radioresistant carrier-specific helper T cells, one could expect that this amplified pool of helper T cells would hasten the development of antibody production by the transferred donor B cells.