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1

Effect of recombinant IFN-gamma on IgE-dependent leukotriene generation by peripheral blood leukocytes in patients with pollinosis and asthma

100%
Krasnowska M., Medrala W., Malolepszy J., Krasnowski R.
Archivum Immunologiae et Therapiae Experimentalis
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2000
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vol. 48
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issue 4
287-292
EN
Interferon gamma (IFN-gamma) is considered one of the causative and intensifying factors in inflammation. The reaction to allergens releases IFN-gamma, an immunomodulatory cytokine known to inhibit IgE synthesis and Th cell proliferation. The aim of the study was to evaluate the influence of IFN-gamma on leukotriene (LT) release in vitro, from human leukocytes of atopic patients with pollinosis and asthma. Thirty-eight patients were enrolled in the study: 15 with pollinosis and 23 asthmatics. In the presence of IL-3, leukocytes were stimulated with specific allergens. Other samples of leukocytes were preincubated with different concentrations of IFN-gamma for 15 min before allergen stimulation. The concentration of LT in supernatants was measured according to the CAST-ELISA procedure. We stated that IFN-gamma had significantly diminished LT release in a dose-dependent mode from the leukocytes of pollinotics. IFN-gamma did not change LT release in the asthmatic group, although, in leukocytes the small and medium basic production of LT, IFN-gamma caused a statistically significant fall in LT generation.
2

Components of the IFN- signaling pathway in tumorigenesis

100%
Blanck G.
Archivum Immunologiae et Therapiae Experimentalis
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2002
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vol. 50
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issue 3
151-158
EN
Many features of the interferon (IFN-) signaling pathway would suggest that it is anti-tumorigenic. The IFN- signaling pathway leads to apoptosis and to the expression of immune function proteins that could cooperate with T cells in the destruction of tumor. Various lines of experimental approaches have in general supported the hypothesis the IFN- signaling pathway is anti-tumorigenic. However, data also indicate that the idea that the IFN- signaling pathway is exclusively anti-tumorigenic is too simplistic. Also, to date, very little of the knowledge regarding the anti-tumor effects of the IFN- pathway has been useful in the prognosis or therapy for cancer. This review summarizes the current state of knowledge regarding the IFN- signaling pathway in tumorigenesis, with an emphasis on MHC class II induction in tumor cells and the induction of apoptosis in tumor cells. The review also indicates some future areas of investigation that offer hope for applying this knowledge in reducing cancer mortality.
3

Differential effects of CD40 stimulation on normal and neoplastic cell growth

100%
Ziebold J. L., Hixon J., Boyd A., Murphy W. J.
Archivum Immunologiae et Therapiae Experimentalis
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2000
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vol. 48
|
issue 4
225-233
EN
CD40 is a molecule in the tumor necrosis factor receptor/nerve growth factor receptor (TNFR/NGFR) family that is present on both normal and neoplastic B lineage cells. It is also expressed on carcinoma and melanoma cells and can be augmented with interferon gamma CD40 stimulation in normal Bcells has been demonstrated to promote normal B cell differentiation and growth in vitro. In contrast to these effects, CD40 stimulation by either anti-CD40 antibodies or a recombinant soluble CD40 ligand can inhibit the growth of human breast carcinomas and aggressive histology B lymphomas in vitro and in vivo. This is believed to occur by activation- -induced cell death (AICD) in which stimuli that promote the growth of normal cell types inhibit the growth of neoplastic counterparts. This occurs through the induction of apoptosis, necrosis and/or cell cycle arrest. Thus, CD40 stimulation may be of potential clinical use in the treatment of carcinomas and B cell lymphomas. This review shall provide an overview of the various effects of CD40 stimulation on both normal and neoplastic cell types.
4

CD80 and CD86 expression on LPS-stimulated monocytes and effect of CD80 and CD86 blockade on IL-4 and IFN-gamma production in nonatopic bronchial asthma

88%
Rutkowski R., Moniuszko T., Stasiak-Barmuta A., Kosztyla-Hojna B., Alifier M., Rutkowski K., Tatarczuk-Krawiel A.
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EN
CD80 and CD86 seem to play an important role in the allergen induced secretion of IL-5 and IL-13. Up till now, the expression of CD80 (B7.1) and CD86 (B7.2) on monocytes and kinetics of these molecules expression on lipopolysaccharide?stimulated monocytes in nonatopic asthma have not been defined. Using monoclonal antibodies we have compared the expression of CD80 (B7.1) and CD86 (B7.2) on monocytes of healthy persons and nonatopic asthmatic patients. We have also assessed the effect of CD80 and CD86 inactivation on interleukin (IL)-4 and interferon gamma (IFN-gamma production in nonatopic asthmatics and healthy subjects. We found that low expression of CD80 on studied monocytes (1.64+0.65 vs. 3.53+1.43%) and moderate expression of CD86 (41.25+134 vs. 49.46+11.49%) were characteristic for asthma. In nonatopic asthma patients inactivation of CD80 or CD86 blockade significantly reduced IFN-gamma production by T lymphocytes (p<0.02; p<0.03). In both studied groups anti-CD80 antibodies did not diminish T lymphocytes` production of IL-4. However anti-CD86 antibodies significantly (p<0.04) reduced the IL-4 concentration in culture supernatants. Our results confirm that both CD80 and CD86 molecules play on important role in the maintenance and amplification of inflammatory process. It suggests that in the inflammatory process that occurs in the nonatopic bronchial asthma Th1 as well as Th2 lymphocytes are equally important
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