In vivo isotype regulation of humoral responses to dextran B1355 in BALB/c mice. Double-class IgG3/IgM producers as a function of age.

This report shows that, in 8- to 10-month-old BALB/c mice immunized intraperitoneally with dextran B1355, approximately 75% of IgG3 anti-alpha (1----3) polyglucan (anti-dex) plaque-forming cells (PFC) detected in the spleen were identified as double-Ig class producers secreting simultaneously IgG3 and IgM antibodies with the same specificity for the dex epitope. Under the same conditions of immunization, however, IgA anti-dex PFC were mostly single-class secretors. IgA PFC developed in the spleen in highest numbers (equal to IgM), but in Peyer's patches IgA PFC were sevenfold more numerous than IgM.

Sensitive radioimmunoassay for the broad-spectrum antiviral agent ribavirin.

Ribavirin, 1-beta-D-ribofuranosyl-1,2,4-triazole-3-carboxyamide (Virazole; Viratek, Inc., Covina, Calif.), has a broad spectrum of antiviral activity.

Age-dependence of the IgA anti-alpha (1 leads to 3) dextran B1355 response in vitro.

The magnitude of the Balb/c mouse IgA anti-alpha (1 leads to 3) dextran B1355 (anti-dex) response in vivo was recently found to be markedly T-cell-dependent and age-dependent. This report demonstrates that the in vitro IgA anti-dex response by mesenteric lymph nodes (MLN) is highly age-dependent and that there is an age-dependent increase of the background IgA anti-dex plaque-forming cell (PFC) response occurring in the absence of added antigen which correlates significantly with the magnitude of the antigen-stimulated response. In aging mice both background and antigen-stimulated IgA anti-dex responses appeared to be significantly higher in MLN than in spleen cultures.

Gluten-sensitive enteropathy. I. The T-dependent anti-A-gliadin antibody response maps to the murine major histocompatibility locus.

We examined the genetic control of the murine humoral immune response to purified A-gliadin, a protein derived from wheat gluten, which is known to cause small intestinal disease in susceptible individuals. Studies with congenic and noncongenic inbred strains of mice revealed that the T-dependent humoral immune response to A-gliadin is under the control of genes mapping to the mouse major histocompatibility complex (MHC). These findings in mice establish a clear linkage between the MHC and the regulation of the immune response to a protein capable of causing human disease.