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Regulation of lymphokine response during reinfection by influenza virus. Production of a factor that inhibits lymphokine activity.

M A Beck and J F Sheridan
J Immunol May 15, 1989, 142 (10) 3560-3567;
M A Beck
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J F Sheridan
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Abstract

Mononuclear cells, obtained from the spleens and lungs of influenza virus-seropositive C57BL/6 mice at 2 to 4 days after re-infection with homologous virus (strain A/Bangkok/1/79), produced a low m.w. factor in vitro that prevents the biologic expression, but not production, of the lymphokine, leukocyte migration inhibition factor (LIF). The low m.w. factor inhibited LIF activity without destroying the LIF molecule inasmuch as simple dialysis restored lymphokine activity to culture supernatants. Production of the low m.w. factor was observed from 2 to 4 days after re-infection, at which time the delayed-type hypersensitivity response to viral Ag was suppressed. In contrast, LIF was produced by splenocytes and lung mononuclear cells obtained at all times tested after re-infection (from 2 to 30 days). Production of the low m.w. factor required re-infection of influenza A virus-seropositive mice with type A virus; re-infection with influenza B virus failed to induce production. Ag specificity was also required in vitro for splenocytes to produce the factor; cells from type A virus-re-infected mice required type A Ag stimulation. Cell depletion studies with mAb plus C revealed that macrophages and T cells along with Ag stimulation were required for factor production by spleen cells. However, mononuclear cells obtained within 4 days from the lungs of re-infected mice did not require in vitro Ag stimulation for production of the low m.w. factor, and factor production was dependent upon the presence of CD4+ (L3T4) cells in the culture. Fractionation of culture supernatants over a Sephadex G-50 column indicated that the factor had a molecular mass of 2 to 3 kDa, and by FPLC chromatofocusing over a Mono P column, the factor eluted at a pH of approximately 8.2. Thus, re-exposure of influenza virus-seropositive mice to homologous virus resulted in the production of a low m.w. factor that prevented the biologic expression of LIF, but not its production. Lymphokines are an important component of the delayed-type hypersensitivity response; the presence of mononuclear cells secreting a low m.w. factor and LIF concomitantly at the site of virus replication (lungs) and the capacity of the factor to block the biologic expression of LIF in vitro suggest that the factor may have a role in the regulation of a delayed-type hypersensitivity response in vivo during re-infection.

  • Copyright © 1989 by American Association of Immunologists

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The Journal of Immunology
Vol. 142, Issue 10
15 May 1989
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Regulation of lymphokine response during reinfection by influenza virus. Production of a factor that inhibits lymphokine activity.
M A Beck, J F Sheridan
The Journal of Immunology May 15, 1989, 142 (10) 3560-3567;

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Regulation of lymphokine response during reinfection by influenza virus. Production of a factor that inhibits lymphokine activity.
M A Beck, J F Sheridan
The Journal of Immunology May 15, 1989, 142 (10) 3560-3567;
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Print ISSN 0022-1767        Online ISSN 1550-6606