Presence of IgE antibodies to bacterial superantigens and increased IL-13-producing T cells in myelitic patients with atopic diathesis.
BACKGROUND
Superantigens are considered to exacerbate autoimmune inflammation through the expansion of autoreactive T cells; however, the immune response to bacterial superantigens has not been extensively studied in any type of myelitis. We recently reported the occurrence of a distinct type of myelitis in patients with atopic diathesis, which in a recent nationwide survey was reported to be widespread in Japan. The aim of this study was to investigate the presence of IgE antibodies to bacterial superantigens and the proportion of IL-13- or IL-5-producing CD4+ or CD8+ T cells in patients with myelitis and atopic diathesis.


METHODS
Twenty-four myelitic patients with and 12 myelitic patients without hyperIgEemia, 28 patients with multiple sclerosis (MS) and 34 healthy controls were enrolled in this study. IgE antibodies to staphylococcal enterotoxins A (SEA) and B (SEB) in sera were measured using a liquid-phase enzyme immunoassay, and the intracellular production of IL-5 and IL-13 in peripheral blood CD4+ and CD8+ T cells was measured by flow cytometry.


RESULTS
The myelitic patients with hyperIgEemia showed significantly higher positive rates of serum SEA/SEB-specific IgE antibodies (41.7 and 62.5%, respectively) than the healthy controls (5.9 and 8.8%), patients with MS (0 and 21.4%) and those with normoIgEemic myelitis (0 and 0%). Moreover, IL-13-producing CD4+ T cells and CD8+ T cells increased significantly in the myelitic patients with hyperIgEemia compared to the controls, while IL-5-producing CD4+ or CD8+ T cells did not.


CONCLUSIONS
The IgE response to staphylococcal superantigens is heightened in myelitic patients with atopic diathesis, which might contribute to increases in IL-13-producing T cells and thus the development of myelitis.
Ochi
Hirofumi
H
Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Osoegawa
Manabu
M
Murai
Hiroyuki
H
Minohara
Motozumi
M
Taniwaki
Takayuki
T
Kira
Jun-Ichi
J
D000328:Adult; D000918:Antibody Specificity / Q000276:immunology; D039741:Antigens, Dermatophagoides / Q000097:blood / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D004198:Disease Susceptibility / Q000276:immunology* / Q000378:metabolism* / Q000628:therapy; D004768:Enterotoxins / Q000097:blood / Q000276:immunology*; D006801:Humans; D007114:Immunization; D007073:Immunoglobulin E / Q000097:blood / Q000276:immunology*; D018793:Interleukin-13 / Q000276:immunology* / Q000378:metabolism*; D015848:Interleukin-5 / Q000276:immunology / Q000378:metabolism; D007564:Japan; D008875:Middle Aged; D009103:Multiple Sclerosis / Q000097:blood / Q000276:immunology; D009187:Myelitis / Q000276:immunology* / Q000378:metabolism* / Q000628:therapy; D013223:Statistics as Topic; D018089:Superantigens / Q000097:blood / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology* / Q000378:metabolism*; D016896:Treatment Outcome
D039741:Antigens, Dermatophagoides; D004768:Enterotoxins; D018793:Interleukin-13; D015848:Interleukin-5; D018089:Superantigens; C026066:enterotoxin A, Staphylococcal; D007073:Immunoglobulin E; C031818:enterotoxin B, staphylococcal