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Immunosuppressive factor from liver induces apoptosis in thymoma EL-4 cells but not normal MHC class II-specific T lymphocytesстатья
Информация о цитировании статьи получена из
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Web of Science
Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 14 октября 2021 г.
- Авторы: Kazansky D.B., Agranovich I.M., Azhipa O.Y., Shtil A.A., Anosova N.G., Chernyshova A.D., Brondz B.D.
- Журнал: Immunology Letters
- Том: 45
- Номер: 1-2
- Год издания: 1995
- Издательство: Elsevier BV
- Местоположение издательства: Netherlands
- Первая страница: 5
- Последняя страница: 11
- DOI: 10.1016/0165-2478(94)00234-I
- Аннотация: An endogenously produced immunosuppressive factor (ISFnp, immunosuppressive factor-neutral protein), inducing a decrease in viability of thymoma EL-4 cells in vitro, was isolated from murine liver using ion exchange, gel filtration and hydrogen-bonding chromatography. Polyclonal rabbit antibodies against this factor were developed and attached to periodate-activated Sepharose CL-6B. The immunoaffine sorbent obtained significantly depleted the biological activity of ISFnp from tested fractions. The factor shows liver-specific location, an Mr of about 70-80 kDa and consists of 2 subunits (40 and 42 kDa) as determined by SDS-PAGE and Western blotting. ISFnp induced DNA degradation in EL-4 cells similar to the cleavage of DNA onto olygonucleosomal fragments in dexamethasone-treated thymocytes. This DNA degradation preceded lysis of thymoma cells, suggesting an induction of apoptosis in ISFnp-treated EL-4 cells. Addition of the factor into primary mixed lymphocyte culture (MLC) strongly inhibited proliferative response but failed to induce any decrease in the ability of normal MHC class II-specific alloreactive cells to respond in the secondary MLC. Moreover, addition of ISFnp into primary MLC on the peak of proliferative response resulted in aug-mentation of secondary responses of primed cells as compared with the same quantities of primed cells from untreated cultures. These results suggest a possible role of liver both in deletion of transformed clones of T lymphocytes and formation of allospecific memory T cells. © 1995.
- Добавил в систему: Казанский Дмитрий Борисович