PMID- 11854206 OWN - NLM STAT- MEDLINE DCOM- 20020401 LR - 20210526 IS - 0019-9567 (Print) IS - 1098-5522 (Electronic) IS - 0019-9567 (Linking) VI - 70 IP - 3 DP - 2002 Mar TI - Recombinant Dirofilaria immitis polyprotein that stimulates murine B cells to produce nonspecific polyclonal immunoglobulin E antibody. PG - 1235-44 AB - Nonspecific immunoglobulin E (IgE) production is an event characteristically observed in parasitic helminth infections, but its mechanisms are still unclear. To define these mechanisms, we prepared a recombinant Dirofilaria immitis protein (rDiAg) and assessed its effect on nonspecific IgE production. rDiAg preferentially induced nonspecific IgE production, without eliciting specific IgE production, as well as a Th2-type cytokine profile (high interleukin-4 [IL-4] and IL-10 production but low gamma interferon production) in BALB/c mice. rDiAg significantly elicited the proliferative response of naive B cells. This response was not abolished by polymyxin B, an inhibitor of lipopolysaccharide (LPS), and rDiAg normally expanded splenic B cells from LPS nonresponder C3H/HeJ mice. Thus, the mitogenic effect of rDiAg was not due to LPS contamination. rDiAg also enhanced levels of CD23 expression on splenic B cells. Splenic B cells produced marked levels of IgE when cultured with the combination of rDiAg and IL-4 (rDiAg-IL-4), whereas peritoneal B cells produced negligible levels of IgE. rDiAg-IL-4-induced IgE production by splenic B cells was synergistically increased by coculture with peritoneal B cells. rDiAg-driven IL-10 secretion was higher in peritoneal B cells than in splenic B cells. IgE production by splenic B cells cocultured with peritoneal B cells was decreased to a level comparable to that by splenic B cells in the presence of a neutralizing anti-IL-10 monoclonal antibody. Collectively, these results suggest that rDiAg-induced polyclonal expansion and IgE class switching of splenic B cells contribute to nonspecific IgE production and that these responses are enhanced by peritoneal B-cell-derived IL-10. FAU - Tezuka, Hiroyuki AU - Tezuka H AD - Section of Environmental Parasitology, Department of International Health Development, Division of Public Health, Graduate School, Tokyo Medical and Dental University, 1-5-45 Yushima Bunkyo-ku, Tokyo 113-8519, Japan. FAU - Imai, Shinjiro AU - Imai S FAU - Muto, Riho AU - Muto R FAU - Furuhashi, Yuko AU - Furuhashi Y FAU - Fujita, Koichiro AU - Fujita K LA - eng PT - Journal Article PL - United States TA - Infect Immun JT - Infection and immunity JID - 0246127 RN - 0 (Antibodies, Helminth) RN - 0 (Antigens, Helminth) RN - 0 (DIPA protein, Dirofilaria immitis) RN - 0 (Helminth Proteins) RN - 130068-27-8 (Interleukin-10) RN - 207137-56-2 (Interleukin-4) RN - 37341-29-0 (Immunoglobulin E) RN - 82115-62-6 (Interferon-gamma) SB - IM MH - Animals MH - Antibodies, Helminth/*blood MH - Antibody Specificity MH - Antigens, Helminth/*immunology MH - B-Lymphocytes/*immunology MH - Cell Differentiation MH - Dirofilaria immitis/*immunology MH - Female MH - Helminth Proteins/*immunology MH - Immunoglobulin Class Switching MH - Immunoglobulin E/*blood MH - Interferon-gamma/blood MH - Interleukin-10/blood MH - Interleukin-4/blood MH - Lymphocyte Activation MH - Male MH - Mice MH - Mice, Inbred BALB C MH - Peritoneal Cavity/cytology MH - Rabbits MH - Spleen/cytology MH - Th2 Cells PMC - PMC127741 EDAT- 2002/02/21 10:00 MHDA- 2002/04/02 10:01 PMCR- 2002/03/01 CRDT- 2002/02/21 10:00 PHST- 2002/02/21 10:00 [pubmed] PHST- 2002/04/02 10:01 [medline] PHST- 2002/02/21 10:00 [entrez] PHST- 2002/03/01 00:00 [pmc-release] AID - 0772 [pii] AID - 10.1128/IAI.70.3.1235-1244.2002 [doi] PST - ppublish SO - Infect Immun. 2002 Mar;70(3):1235-44. doi: 10.1128/IAI.70.3.1235-1244.2002.