| http://purl.uniprot.org/citations/8879221 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/8879221 | http://www.w3.org/2000/01/rdf-schema#comment | "CD4+ and CD8+ alpha/beta+ T cells of the T helper cell (Th)2 phenotype produce the cytokines IL-4, IL-5, and IL-13 that promote IgE production and eosinophilic inflammation. IL-4 may play an important role in mediating the differentiation of antigenically naive alpha/beta+ T cells into Th2 cells. Murine NK1.1+ (CD4+ or CD4-CD8-) alpha/beta+ T cells comprise a beta 2-microglobulin (beta 2m)-dependent cell population that rapidly produces IL-4 after cell activation in vitro and in vivo and has been proposed as a source of IL-4 for Th2 cell differentiation. alpha/beta+ CD8+ T cells, most of which require beta 2m for their development, have also been proposed as positive regulators of allergen-induced Th2 responses. We tested whether beta 2m-dependent T cells were essential for Th2 cell-mediated allergic reactions by treating wild-type, beta 2m-deficient (beta 2m -/-), and IL-4-deficient (IL-4 -/-) mice of the C57BL/6 genetic background with ovalbumin (OVA), using a protocol that induces robust allergic pulmonary disease in wild-type mice. OVA-treated beta 2m -/-mice had circulating levels of total and OVA-specific IgE, pulmonary eosinophilia, and expression of IL-4, IL-5, and IL-13 mRNA in bronchial lymph node tissue similar to that of OVA-treated wild-type mice. In contrast, these responses in OVA-treated IL-4 -/-mice were all either undetectable or markedly reduced compared with wild-type mice, confirming that IL-4 was required in this allergic model. These results indicate that the NK1.1+ alpha/beta+ T cell population, as well as other beta 2m-dependent populations, such as most peripheral alpha/beta+ CD8+ T cells, are dispensable for the Th2 pulmonary response to protein allergens."xsd:string |
| http://purl.uniprot.org/citations/8879221 | http://purl.org/dc/terms/identifier | "doi:10.1084/jem.184.4.1507"xsd:string |
| http://purl.uniprot.org/citations/8879221 | http://purl.uniprot.org/core/author | "Zhang Y."xsd:string |
| http://purl.uniprot.org/citations/8879221 | http://purl.uniprot.org/core/author | "Lewis D.B."xsd:string |
| http://purl.uniprot.org/citations/8879221 | http://purl.uniprot.org/core/author | "Rogers K.H."xsd:string |
| http://purl.uniprot.org/citations/8879221 | http://purl.uniprot.org/core/date | "1996"xsd:gYear |
| http://purl.uniprot.org/citations/8879221 | http://purl.uniprot.org/core/name | "J Exp Med"xsd:string |
| http://purl.uniprot.org/citations/8879221 | http://purl.uniprot.org/core/pages | "1507-1512"xsd:string |
| http://purl.uniprot.org/citations/8879221 | http://purl.uniprot.org/core/title | "Beta 2-microglobulin-dependent T cells are dispensable for allergen-induced T helper 2 responses."xsd:string |
| http://purl.uniprot.org/citations/8879221 | http://purl.uniprot.org/core/volume | "184"xsd:string |
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