Роль гликопротеидов, регулирующих апоптоз, в дифференцировке гемопоэтических клеток человека тема диссертации и автореферата по ВАК РФ 14.00.14, доктор биологических наук Заботина, Татьяна Николаевна
Заботина, Татьяна Николаевна
доктор биологических наук
2005
- Специальность ВАК РФ14.00.14
- Количество страниц 276
Оглавление диссертации доктор биологических наук Заботина, Татьяна Николаевна
Содержание.
Список сокращений.
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Введение диссертации (часть автореферата) на тему «Роль гликопротеидов, регулирующих апоптоз, в дифференцировке гемопоэтических клеток человека»
Актуальность темы.6
Цель работы.9
Задачи исследования.10
Научная новизна.10
Научно-практическая значимость.11
ЧАСТЬ I. ОБЗОР ЛИТЕРАТУРЫ.12
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Заключение диссертации по теме «Онкология», Заботина, Татьяна Николаевна
228 ВЫВОДЫ
1. CD95 является дифференцировочным антигеном лейкоцитов человека, следовательно, его экспрессия связана с определенными этапами созревания лимфоидных и миелоидных гемопоэтических клеток.
2. Среди CD45+/CD14" лимфоцитов периферической крови взрослых доноров антиген CD95 определяется на 35-75% клеток, из них 40-60% составляют СОЗ+Т-клетки, а также на всех CD 19+В-клетках. На тимоцитах рецептор CD95 представлен на 8,7±35,2% клеток.
3. Антиген CD95 отсутствует на моноцитах и гранулоцитах во всех образцах периферической крови здоровых доноров независимо от возраста. В то же время, экспрессия антигена CD95 на CD45+/CD14" лимфоидных клетках зависит от возраста и отсутствует на лимфоцитах периферической крови только новорожденных детей.
4. На ранних этапах дифференцировки В-клеток (пре-пре-В ОЛЛ) антиген CD95 коэкспрессирован на СБ19+клетках. На поздних этапах дифференцировки CD19+, HLA-Dr+, CD5+ В-клетках (В-ХЛЛ) антиген CD95 отсутствует при всех стадиях развития заболевания.
5. Коэкспрессия на бластных клетках больных ХМЛ молекулы CD95 и дифференцировочных антигенов CD13, CD33 свидетельствует о том, что он является маркером ранних этапов миелоидной дифференцировки. На полиморфноядерных клетках миелоидного ряда антиген CD95 отсутствует на всех стадиях ХМЛ.
6. В стадии бластного криза ХМЛ у 32% больных выявляется функционально активный белок CD243, экспрессирующийся на CD34+, CD33+, CD13+ клетках.
7. На CD45+-лимфоидных клетках периферической крови здоровых доноров антиген CD243 отсутствует на мембране CD3+ Т-лимфоцитов, однако, все CD19+ В-лимфоциты его экспрессируют в функционально неактивном состоянии. Белок CD243 обнаружен также на 10-30% тимоцитов.
8. Экспрессия Bcl-2 меняется на этапах дифференцировки В-клеток. Bcl-2 экспрессируется на стадии зрелых периферических В-клеток и отсутствует в ранних В-клетках и плазматических клетках.
9. Тимоциты с фенотипом CD4+/CD8", CD4"/CD8+, CD47CD8" , а также CD3+/Ki-67+, CD3+/Ki-67" Т-клетки и CD19+/Ki-67" В-клетки лимфатических узлов обладают высокой экспрессией Bcl-2. Белок Bcl-2 отсутствует на части тимоцитов с фенотипом CD4+/CD8+ и в CD 19+/Ki-67+ В-клетках лимфатических узлов.
Ю.Высокая экспрессия белка Bcl-2 наблюдается в митохондриях лейкозных CD5+, CD19+, HLA-Dr+ В-клеток периферической крови больных B-XJIJI как на ранних, так и в развернутых стадиях развития заболевания.
11.Отсутствие CD95 на В-клетках больных ХЛЛ и, выявленная двумя методами (пропидий иодид и TUNEL) специфическая фрагментация ДНК клеток в процессе терапии, свидетельствует о С095-рецепторно-независимом механизме апоптоза при данной форме лимфопролиферативного заболевания.
12.Судьба гемопоэтической клетки в процессе дифференцировки зависит от соотношения антиапоптотических и проапоптотических белков. Перспектива развития заболевания и прогностическая ценность использованных маркеров может быть оценена только при их комплексном анализе.
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