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Lack of Fc receptor for IgE in SJA9 mice

✍ Scribed by Mitsunobu Adachi; Ko Okumura; Naohiro Watanabe; Nobuhiro Noro; Tohru Masuda; Junji Yodoi


Publisher
Springer-Verlag
Year
1985
Tongue
English
Weight
457 KB
Volume
22
Category
Article
ISSN
0093-7711

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✦ Synopsis


In allergic patients and rodents infected with the nematode, Nippostrongylus brasiliensis (Nb), enhancement of IgE production is associated with a marked increase in lymphocytes bearing the Fc receptor specific for IgE (Fc~R) as detected by the rosetting method (Saxon et al. 1980, Ishizaka et al. 1976). In vitro studies also showed that IgE production is regulated by T cells expressing Fc~R via production of soluble factors (IgE-binding factors; Yodoi et al. 1979, 1980, Ishizaka et al. 1981).

SJA9 (SJA) mice, an allotype congenic strain of SJL, cannot produce IgE antibody even after infection with Nb (Borges et al. 1981). To analyze the mechanism of feedback regulation between IgE production and Fc~R on lymphocytes, we studied Fc~R regulation in SJA mice. In noninfected SJA mice, Fc~R was expressed on less than 5% of the total spleen cells as was the case in noninfected control strains. Although 13-20% of spleen cells expressed Fc,R after the infection in control mice, Fc~R was expressed on only 3.1-2.9% of the total cells in the SJA strain. Abnormality of F%R inducibility by IgE was also confirmed in vitro.

The proportion of spleen cells expressing Fc~R was determined by rosette formation with fixed ox red blood cells (Eo') coated with mouse hybridoma IgE" (Eo'-IgE) using the technique described elsewhere (Yodoi et al. 1979). In SJA as well as control strains (BALB/c, SJL), the proportion of Fc~R(+ ) cells in normal spleen cells was less than 5%. As predicted from the data on Nb-infected rats, more than 20% of BALB/c spleen cells formed rosettes with Eo'-IgE 7-10 days after Nb infection. In contrast, less than 6% (3.1 _+2.9%) of Nb-infected SJA spleen cells formed rosettes (Fig. 1). In Nb-infected SJA mice, therefore, there appeared to be neither an enhancement of IgE production nor an increase of F%R(+) cells.

To confirm the specificity of Fc,R on mouse lymphocytes, we examined the specificity of rosette formation with Eo'-IgE. Since the proportion of rosetteforming cells was low in Nb-infected SJA mice, we used spleen cells from Nbinfected SJL mice, which are known to show subnormal IgE production after infection. In contrast to SJA mice, there was a sevenfold increase of rosette-forming cells after Nb infection in SJL mice (Fig. 2). The cells from infected mice were


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