期刊
JOURNAL OF IMMUNOLOGY
卷 176, 期 12, 页码 7272-7277出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.176.12.7272
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资金
- NHLBI NIH HHS [R01 HL088297, K08 HL072775] Funding Source: Medline
- NIAID NIH HHS [AI46731, AI27849] Funding Source: Medline
- NIDDK NIH HHS [P30 DK040561, P30 DK040561-11, DK43351] Funding Source: Medline
CARMA1 has been shown to be important for Ag-stimulated activation of NF-kappa B in lymphocytes in vitro and thus could be a novel therapeutic target in inflammatory diseases such as asthma. In the present study, we demonstrate that mice with deletion in the CARMA1 gene (CARMA1(-/-)) do not develop inflammation in a murine model of asthma. Compared with wild-type controls, CARMA1(-/-) mice did not develop airway eosinophilia, had no significant T cell recruitment into the airways, and had no evidence for T cell activation in the lung or draining lymph nodes. In addition, the CARMA1(-/-) mice had significantly decreased levels of IL-4, IL-5, and IL-13, did not produce IgE, and did not develop airway hyperresponsiveness or mucus cell hypertrophy. However, adoptive transfer of wild-type Th2 cells into CARMA1(-/-) mice restored eosinophilic airway inflammation, cytokine production, airway hyperresponsiveness, and mucus production. This is the first demonstration of an in vivo role for CARMA1 in a disease process. Furthermore, the data clearly show that CARMA1 is essential for the development of allergic airway inflammation through its role in T lymphocytes, and may provide a novel means to inhibit NF-kappa B for therapy in asthma.
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