IgE formation and Fc receptor-positive lymphocytes in normal, immuno-deficient, and auto-immune mice infected with Nippostrongylus brasiliensis.
The IgE serum levels and IgE FcR-positive lymphocytes (Fc epsilon R) in the spleen and mesenteric lymph nodes (MLN) of normal and immunologically mutant strains of mice were determined before and 14 days after infection with Nippostrongylus brasiliensis (Nbr) parasites. By IgE rosetting of cells immunofluorescently stained for sIg. Thy-1.2, Lyt-2, and L3T4, only sIg+ IgE rosetting lymphocytes were detected in both normal and Nbr-infected mice. IgE high responder mice had the same percentage of Fc epsilon R+ spleen and MLN lymphocytes as low responder mice. After Nbr infection, the percentages of splenic and MLN Fc epsilon R+ cells increased in parallel to a similar increase of sIg+ B cells. Athymic C57BL/6J-nu mice had 62% Fc epsilon R+ spleen and 85% Fc epsilon R+ MLN cells before and after Nbr infection, but IgE serum levels were less than 5 ng IgE/ml. C57BL/6J mice with the viable moth-eaten mutation mev which have almost exclusively Ly-1+ B cells, had less than 1% Fc epsilon R+ lymphocytes and formed only small amounts of IgE. C57BL/6J mice with the lymphoproliferation (lpr) or generalized lymphoproliferative disease (gld) mutations had low numbers of Fc epsilon R+ cells but formed 15 to 30 times more IgE after Nbr infection than control C57BL/6J mice. The IgE response of mice with the beige mutation (bg) did not differ from control mice. Mice with the xid mutation had few Fc epsilon R+ and sIg+ cells but showed high IgE responses. These data demonstrate that Fc epsilon R are typical cell surface markers for approximately 90% of murine Ly-1-, sIg+ B cells and that the number of Fc epsilon R+ cells does not correlate with the capacity of the mice to form IgE. The IgE response to Nbr infection is normal in mice homozygous for the bg mutation, elevated in mice homozygous for the xid, lpr, and gld mutations, and decreased in mice homozygous for the mev and nu mutations.
Lebrun
P
P
Department of Immunology, Research Institute of Scripps Clinic, La Jolla, CA 92037.
Sidman
C L
CL
Spiegelberg
H L
HL
D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology* / Q000378:metabolism; D002469:Cell Separation; D005260:Female; D007073:Immunoglobulin E / Q000032:analysis / Q000096:biosynthesis*; D007074:Immunoglobulin G / Q000145:classification; D007075:Immunoglobulin M / Q000032:analysis; D007153:Immunologic Deficiency Syndromes / Q000276:immunology* / Q000378:metabolism; D008214:Lymphocytes / Q000145:classification / Q000378:metabolism*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D008808:Mice, Inbred CBA; D009349:Nematode Infections / Q000097:blood / Q000276:immunology* / Q000378:metabolism; D009559:Nippostrongylus; D010641:Phenotype; D011961:Receptors, Fc / Q000032:analysis*; D017455:Receptors, IgE; D012397:Rosette Formation / Q000379:methods
D007074:Immunoglobulin G; D007075:Immunoglobulin M; D011961:Receptors, Fc; D017455:Receptors, IgE; D007073:Immunoglobulin E