TY - JOUR
T1 - Induction of antigen-specific IgE response in murine lymphocytes by IL-10
AU - Ohmori, Hitoshi
AU - Kanda, Tsutomu
AU - Takai, Toshiyuki
AU - Hikida, Masaki
N1 - Copyright:
Copyright 2015 Elsevier B.V., All rights reserved.
PY - 1995
Y1 - 1995
N2 - When murine spleen cells that had been primed with trinitrophenyl-keyhole limpet hemocyanin (TNP-KLH) were stimulated in vitro with the same antigen, anti-TNP IgE, as well as anti-TNP IgM and IgG1, was secreted into the culture medium. On the other hand, anti-TNP IgM and IgG1 were produced, but anti-TNP IgE secretion was negligible when the carrier (KLH)-primed spleen cells were cultured with the hapten-carrier antigen (TNP-KLH) under the same conditions. Anti-TNP Ig responses in the latter cultures are thought to reflect the interaction between normal TNP-specific B cells and KLH-primed helper T cells. By using this culture system, we investigated the requirements of exogenous cytokines for inducing anti-TNP IgE response. The addition of interleukin-4 (IL-4), that is known to induce IgE response in LPS-stimulated murine B cells, failed to elicit anti-TNP IgE response. The combination of IL-4 with IL-2 and/or IL-5 was also ineffective. Interestingly, a significant level of anti-TNP IgE was induced when IL-10, another cytokine from type 2 helper T cells, was added to the culture. Although IL-10 enhanced the production of anti-TNP IgM and IgG1, as well as that of anti-TNP IgE, the rate of enhancement was at least 3-fold higher in the IgE response than in the IgM and IgG1 responses. Simultaneous addition of IL-4, IL-5 or IL-13 with IL-10 did not augment but rather reduced the enhancing effects of IL-10. IL-10 did not further stimulate the spontaneous secretion of IgE from antigen-primed B cells. These results suggest that IL-10 plays a positive role in the induction of antigen-specific IgE responses.
AB - When murine spleen cells that had been primed with trinitrophenyl-keyhole limpet hemocyanin (TNP-KLH) were stimulated in vitro with the same antigen, anti-TNP IgE, as well as anti-TNP IgM and IgG1, was secreted into the culture medium. On the other hand, anti-TNP IgM and IgG1 were produced, but anti-TNP IgE secretion was negligible when the carrier (KLH)-primed spleen cells were cultured with the hapten-carrier antigen (TNP-KLH) under the same conditions. Anti-TNP Ig responses in the latter cultures are thought to reflect the interaction between normal TNP-specific B cells and KLH-primed helper T cells. By using this culture system, we investigated the requirements of exogenous cytokines for inducing anti-TNP IgE response. The addition of interleukin-4 (IL-4), that is known to induce IgE response in LPS-stimulated murine B cells, failed to elicit anti-TNP IgE response. The combination of IL-4 with IL-2 and/or IL-5 was also ineffective. Interestingly, a significant level of anti-TNP IgE was induced when IL-10, another cytokine from type 2 helper T cells, was added to the culture. Although IL-10 enhanced the production of anti-TNP IgM and IgG1, as well as that of anti-TNP IgE, the rate of enhancement was at least 3-fold higher in the IgE response than in the IgM and IgG1 responses. Simultaneous addition of IL-4, IL-5 or IL-13 with IL-10 did not augment but rather reduced the enhancing effects of IL-10. IL-10 did not further stimulate the spontaneous secretion of IgE from antigen-primed B cells. These results suggest that IL-10 plays a positive role in the induction of antigen-specific IgE responses.
KW - Antigen-specific IgE
KW - Interleukin-10
KW - Interleukin-4
KW - Murine lymphocyte
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U2 - 10.1016/0165-2478(95)00084-I
DO - 10.1016/0165-2478(95)00084-I
M3 - Article
C2 - 8537089
AN - SCOPUS:0029149367
VL - 47
SP - 127
EP - 132
JO - Immunology Letters
JF - Immunology Letters
SN - 0165-2478
IS - 1-2
ER -