Regulation of reaginic antibody production in mice. I. Suppression by antigen of IgE antibody production in vitro.

Abstract

Regulation of IgE production by antigen in a primed murine splenic lymphocyte culture system was described. Maximum IgE antibody production was found to occur when cells were cultured in the absence of exogenously added antigen. A cells and T lymphocytes did not affect the production of anti-DNP IgE antibody. By using a hapten-carrier antigen system (DNP-EA) for priming mice in vivo, it was found that the production of anti-DNP IgE by spleen cells in vitro was inhibited by hapten when coupled to homologous (EA) or heterologous (BGG) carrier, and was not enhanced or inhibited by homologous carrier. Anti-DNP IgE antibody production by cultures depleted of macrophages or T lymphocytes was found to be as sensitive to the suppressive effects of hapten as was the IgE production by whole spleen cell cultures. Both IgM and IgG secondary anti-DNP PFC responses in vitro were enhanced by the presence of the homologous hapten-carrier or carrier alone. DNP-BGG had no effect on the anti-DNP IgM or IgG PFC responses of the cultures. These data suggest that endogenous production of antibody (IgM or IgG) was not responsible for the observed suppression of the IgE response in vitrol The experimental results presented indicate that the regulation of the IgE production by antigen in the primed mouse splenic lymphocyte cultures was a consequence of the direct interaction of hapten with IgE B cells.

Pollen-Allergen IgE Response in the Inbred Rat

“…Some previous works have indicated [10,22] either that different T and B cells subsets were in volved in the synthesis of IgG and IgE anti bodies, or that IgG and IgE antibody B-forming cells might differ in their reactiv ity versus a same T helper cell. IgE anti body synthesis can be suppressed in vitro or in vivo by antigen-specific or class-specific factors [7,14,19,20]. Indeed, in rats, Tada [20] showed that the IgE response is short lived and hardly boosterable [reviewed by Jarrett,9].…”

BMX-ARHGAP fusion protein maintains the tumorigenicity of gastric cancer stem cells by activating the JAK/STAT3 signaling pathway

“…The cell lysates were separated using a sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE), with the isolated protein being transferred onto a polyvinylidene fluoride (PVDF) membrane set to a constant voltage of 80 V. Followed by 1-h of blocking, the membrane was incubated with diluted primary antibodies overnight at 4 °C. The primary antibodies against BMX-ARHGAP and against polyclonal antibody BMX-SH were obtained from the mice immunized as previously described [20]. The primary antibodies used included antibodies for BMX (ab207559, 1:500–1000), ARHGAP (ab74454, 1:500–1000), CD133 (ab216323, 1:1000), CD44 (ab157107, 1:2000), SOX2 (ab92494, 1:1500), JAK2 (ab200783, 1:5000), p-JAK2 (ab32101, 1:2000), STAT3 (ab68153, 1:1500), p-STAT3 (ab76315, 1:2000), Nanog (ab80892, 1:1000) and GAPDH (ab181602, 1:5000).…”

Concepts of the Pathogenesis of Allergic Disease: Possible Roles of Epstein–Barr Virus Infection and Interleukin–2 Production

“…Danneman and Michael [19]showed that mouse spleen cells obtained 10–11 days after primary immunization with alum–absorbed antigen formed both IgE and IgG antibodies in culture, and that T cells were not involved in antibody formation. In view of the similarities between their findings and our observations, we cultured antigen–primed cells in microtiter plates.…”