Страница: 7/9
1твие на эффективность клеточной защиты. От преобладания того
1или иного из этих цитокинов могут зависеть исход инфекции и эф-
1фективность противоопухолевой защиты. /2461к/
4. Индуцирует продукцию гамма-ИФ Т-лимфоцитами. Усиливает про-
лиферацию лимфоцитов в ответ на митогены. Потенцирует действи-
еИЛ-2. /2460к/95/
- Усиливает действие вакцины против лейшманиоза. /2460к/95/
1Последствия удаления генов цитокинов
1или их рецепторов /2317к/97/
1───────────────────────────────────────────────────────────────
1Цитокин, │ Ожидаемые последствия │ Неожиданные
1рецепторы│ │ последствия
1───────────────────────────────────────────────────────────────
1ИЛ-12 Ослабление образования Тh1
Лечение инфеционных заболеваний. /2356к/
1───────────────────────────────────────────────────────────────
.
ИЛ-13 9- Т-лимфоциты _Противовоспалительный агент
17 (Тх2)
Эффекты:
1. Противовоспалительный агент
_Стимуляция синтеза
- рецепторного антагониста ИЛ-1 (РАИЛ);
_Подавляет образование . провоспалительных цитокинов. По харак-
теру влияния очень близок к ИЛ-4. /2461к/
- ИЛ-1, ИЛ-6,
- ФНО
5Индукция п-ИФ продукции РВ2, Т- и ЕКК ИЛ-6, ИЛ-1, ФНО. - ???
2. Стимулирует пролиферацию _стволовых клеток ., дифференцировку
моноцитов. /2300к/
3. Хемоаттрактор для моноцитов.
4. Ингибирует противопаразитарную активность, токсичность, мак-
рофаг-связанную иммуносупрессию. /2460к/
.
ИЛ-15
Эффекты:
1. Активирует ЕКК, пролиферацию Т-лимфоцитов, их дифференциров-
ку в Тк. /2460к/ Инициирует образование лимфокинактивирован-
ных киллеров. /2460к/95/
───────────────────────────────────────────────────────────────
Примечание: ЭК - эндотелиальные клетки
рэс - ретикулоэндотелиальная система
ФНО - фактор некроза опухолей
ИФ - интерферон
ЕКК - естественные клетки-киллеры
Pg - простагландины
ФАТ - фактор активации тромбоцитов
.
Oppenheimer-Marks N. Brezinschek RI. Mohamadzadeh M. Vita R. Lipsky
PE.
_Interleukin 15 . is produced by endothelial cells and increases the
transendothelial migration of T cells In vitro and in the SCID mouse-human
rheumatoid arthritis model In vivo.
Source
Journal of Clinical Investigation. 101(6):1261-72, 1998 Mar 15.
The capacity of endothelial cells (EC) to produce IL-15 and the capacity
of IL-15 to influence transendothelial migration of T cells was examined.
Human umbilical vein endothelial cells expressed both IL-15 mRNA and
protein. Moreover, endothelial-derived IL-15 enhanced transendothelial
migration of T cells as evidenced by the inhibition of this process by
blocking monoclonal antibodies to IL-15. IL-15 enhanced transendothelial
migration of T cells by activating the binding capacity of the integrin
adhesion molecule LFA-1 (CD11a/CD18) and also increased T cell motility.
In addition, IL-15 induced expression of the early activation molecule
CD69. The importance of IL-15 in regulating migration of T cells in vivo
was documented by its capacity to enhance accumulation of adoptively
transferred human T cells in rheumatoid arthritis synovial tissue
engrafted into immune deficient SCID mice. These results demonstrate that
EC produce IL-15 and imply that endothelial IL-15 plays a critical role in
stimulation of T cells to extravasate into inflammatory tissue.
Lantero S. Sacco O. Scala C. Rossi GA.
Stimulation of blood mononuclear cells of atopic children with the
relevant allergen induces the release of eosinophil chemotaxins such as
_IL-3, IL-5, and GM-CSF.
Journal of Asthma. 34(2):141-52, 1997.
Peripheral blood mononuclear cells (PBMC) from 10 atopic asthmatic
children (atopics), sensitized to Dermatophagoides pteronyssinus (Dp), and
from 5 nonatopic healthy children (controls) were stimulated with Dp
extract or with birch extract (Be). After 6 days we tested the
supernatant's (Sn) chemotactic activity toward purified blood
eosinbnophils and T-lymphocyte proliferation. Dp induced a statistically
significant T-cell proliferation from atopics as compared to controls (p <
0.05), which correlated with the levels of eosinophil chemotactic activity
in the Sn (r = 0.713; p < 0.05). Measurable levels of IL-3, IL-5, and
GM-CSF were demonstrated in the Sn of Dp-stimulated PBMC from atopics,
while eosinophil locomotion toward different concentrations of recombinant
human (rh) IL-3, rhIL-5, and rhGM-CSF confirmed that these cytokines were
able to stimulate eosinophil chemotaxis in a close concentration range.
Preincubation of different concentrations of the same Sn with blocking
antisera demonstrated that anti-human (ah) IL-3, ahIL-5, and ahGM-CSF
effectively decreased eosinophil chemotaxis (p < 0.05; each comparison).
Thus PBMC activation with the relevant allergen induces the release by T
cells with a Th2 phenotype of chemotactic factors for eosinophils.
Ogawa M. Tsutsui T. Zou JP. Mu J. Wijesuriya R. Yu WG. Herrmann S.
Kubo T. Fujiwara H. Hamaoka T.
Enhanced induction of very late antigen 4/lymphocyte function-associated
_antigen 1-dependent T-cell migration to tumor sites following
_administration of interleukin 12.
Cancer Research. 57(11):2216-22, 1997 Jun 1.
Administration of interleukin 12 (IL-12) into mice bearing CSA1M, OV-HM,
Meth A, or MCH-1-A1 tumor induced complete regression of CSA1M and OV-HM
tumors but induced only a slight growth inhibition of Meth A and MCH-1-A1
tumors. These effects of IL-12 were associated with high and only marginal
levels of T-cell infiltration into CSA1M/OV-HM and Meth A/MCH-1-A1 tumor
masses, respectively. Here, we investigated the role of IL-12 in the
induction of T-cell migration. Spleen cells from untreated or
IL-12-treated CSA1M-bearing mice were stained in vitro with a fluorescein
chemical and transferred i.v. into IL-12-untreated CSA1M-bearing mice.
Migration of donor cells was quantitated by counting the number of
fluorescent cells on cryostat sections of tumor masses. Although only a
slight migration was detected for spleen cells from IL-12-untreated
CSA1M-bearing as well as IL-12-treated or untreated normal mice, enhanced
migration was observed for cells from IL-12-treated CSA1M-bearing mice. A
similar enhanced migration was observed for the OV-HM model. In contrast,
such an enhancement was only marginal in the Meth A and MCH-1-A1 models.
Immunohistochemical studies of tumors from IL-12-treated mice revealed
that the predominant T-cell subset was CD4+ in CSA1M and CD8+ in OV-HM
tumor masses. Consistent with this observation, the dominant subset of
migrating T cells was found to be CD4+ in the CSA1M and CD8+ in the OV-HM
models. T-cell migration was inhibited by pretreatment of recipients with
either combination of anti-very late antigen 4 + anti-vascular cell
adhesion molecule 1 or anti-lymphocyte function-associated antigen 1 +
anti-intercellular adhesion molecule 1 monoclonal antibody. These results
indicate that IL-12 can confer T cells with a capacity to migrate to tumor
sites through very late antigen 4/lymphocyte function-associated antigen 1
adhesion pathways and that the in vivo acquisition of such a capacity
following IL-12 treatment correlates with the induction of tumor
regression.
Marth T. Strober W. Seder RA. Kelsall BL.
Regulation of transforming growth factor-beta production by
Реферат опубликован: 11/04/2005 (17832 прочтено)