Antigen-induced increases in pulmonary mast cell progenitor numbers depend on IL-9 and CD1d-restricted NKT cells.
Antigen-induced increases in pulmonary mast cell progenitor numbers depend on IL-9 and CD1d-restricted NKT cells.
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DOI：
10.4049/jimmunol.0901471
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发表时间：
2009-10-15
期刊：
影响因子：
--
通讯作者：
Gurish MF
中科院分区：
文献类型：
--
作者：
Jones TG;Hallgren J;Humbles A;Burwell T;Finkelman FD;Alcaide P;Austen KF;Gurish MF
致敏和雾化银攻击小鼠的肺肥大细胞祖细胞（MCp）数量急剧增加。这种增加取决于CD 4 + T细胞，因为在气溶胶Ag激发前，在CD 4+而不是CD 8+细胞的mAb耗竭后，致敏野生型（WT）小鼠的肺中未发生MCp增加。在WT小鼠中，在Ag激发前，IL-4、IL-4 R α链、STAT-6、IFN-γ或IL-12 p40的遗传缺失或IFN-γ、IL-3、IL-4、IL-5、IL-6、IL-10、IL-13、IL-17 A、IL-12 p40或IL-12 p40 R β1的mAb阻断均未降低肺MCp升高。然而，致敏和Ag激发的IL-9缺陷小鼠和致敏的WT小鼠在Ag激发前给予IL-9 mAb，分别显示诱导的肺MCp/106单核细胞显著减少47%和66%。在Ag激发前接受抗CD 1d的CD 1d缺陷小鼠和WT小鼠也显示，诱导的肺MCp/106单核细胞分别显著减少65%和59%，揭示了MCp募集的额外要求。然而，在Jα18缺陷小鼠中，仅缺乏1型或不变的NKT细胞，用Ag激发的肺MCp数量的增加是完整的，表明它们的募集必须由2型NKT细胞介导。此外，IL-9缺陷小鼠的抗-CD 1d治疗或CD 1d缺陷小鼠的抗-IL-9治疗不能进一步减少单一缺陷发生的MCp募集的显著部分损害。这些发现暗示2型NKT细胞和IL-9作为在介导Ag诱导的肺MCp数量增加的相同途径中起作用的中枢调节因子。
Pulmonary mast cell progenitor (MCp) numbers increase dramatically in sensitized and aerosolized Ag-challenged mice. This increase depends on CD4+ T cells, as no MCp increase occurs in the lungs of sensitized wild-type (WT) mice after mAb depletion of CD4+ but not CD8+ cells before aerosol Ag challenge. Neither the genetic absence of IL-4, IL-4Rα chain, STAT-6, IFN-γ, or IL-12p40 nor mAb blockade of IFN-γ, IL-3, IL-4, IL-5, IL-6, IL-10, IL-13, IL-17A, IL-12p40, or IL-12p40Rβ1 before Ag challenge in WT mice reduces the pulmonary MCp increase. However, sensitized and Ag-challenged IL-9-deficient mice and sensitized WT mice given mAb to IL-9 just before Ag challenge show significant reductions in elicited lung MCp/106 mononuclear cells of 47 and 66%, respectively. CD1d-deficient mice and WT mice receiving anti-CD1d before Ag challenge also show significant reductions of 65 and 59%, respectively, in elicited lung MCp/106 mononuclear cells, revealing an additional requirement for MCp recruitment. However, in Jα18-deficient mice, which lack only type 1 or invariant NKT cells, the increase in the numbers of lung MCp with Ag challenge was intact, indicating that their recruitment must be mediated by type 2 NKT cells. Furthermore, anti-CD1d treatment of IL-9-deficient mice or anti-IL-9 treatment of CD1d-deficient mice does not further reduce the significant partial impairment of MCp recruitment occurring with a single deficiency. These findings implicate type 2 NKT cells and IL-9 as central regulators that function in the same pathway mediating the Ag-induced increase in numbers of pulmonary MCp.
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影响因子：
64.8
作者：
Bettelli, E;Carrier, YJ;Kuchroo, VK
通讯作者：
Kuchroo, VK
DOI：
10.1084/jem.160.1.12
发表时间：
1984-07-01
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Guy-Grand D;Dy M;Luffau G;Vassalli P
通讯作者：
Vassalli P
影响因子：
4.4
作者：
Ikeda, RK;Miller, M;Broide, DH
通讯作者：
Broide, DH
影响因子：
1.6
作者：
KAMIYA, M;OKU, Y;OHBAYASHI, M
通讯作者：
OHBAYASHI, M
影响因子：
64.5
作者：
HUANG, E;NOCKA, K;BESMER, P
通讯作者：
BESMER, P