مورد إلكتروني

Regulation of CD1d-Medicated Antigen Presentation by Nf1

التفاصيل البيبلوغرافية
العنوان: Regulation of CD1d-Medicated Antigen Presentation by Nf1
المصدر: DTIC
بيانات النشر: 2012-02
تفاصيل مُضافة: INDIANA UNIV INDIANAPOLIS
Brutkiewicz, Randy
نوع الوثيقة: Electronic Resource
مستخلص: The goal of this Exploration-Hypothesis Development Award is to analyze the role of NF1 in the functional expression of CD1d. During the second year of the award, we have analyzed the ability of bone marrow-derived dendritic cells (BMDC) from wildtype (WT) and NF1+/- mice to stimulate fresh NKT cells. The original hypothesis was that we would observe more Th2 (i.e., anti-inflammatory)--as opposed to Th1 (i.e., pro-inflammatory)--cytokine production by NKT cells. Our results suggest that NKT cells from both WT and NF1+/- mice can produce both Th1 and Th2 cytokines at comparable levels. As indicated last year, when analyzing the level of cell surface CD1d, it was observed that BMDC generated from NF1+/- mice expressed 75% of the WT level of CD1d, but were able to stimulate NKT cells as well as those from WT mice. However, we have found a reduction in a B220+CD1d-hi population in splenocytes from NF1 +/- mice. This suggests that NF1 plays an important role in the qualitative expression of CD1d. Furthermore, NKT cells from NF1+/- mice are more activated at baseline, than those from WT mice. In line with this observation, RMA/S tumor growth in NF1+/-mice was reduced compared to WT mice. Therefore, these data strongly suggest that NF1 plays an important (albeit inhibitory) role in the host s innate antitumor immune response (i.e., CD1d/NKT cell axis)
The original document contains color images.
مصطلحات الفهرس: Medicine and Medical Research, ANTIGENS, CYTOKINES, CELLS(BIOLOGY), GROWTH(PHYSIOLOGY), HYPOTHESES, MICE, NEOPLASMS, OBSERVATION, SKILLS, BMDC(BONE MARROW DERIVED DENDRITIC CELLS), NEUROFIBROMATOSIS TYPE 1, ANTIGEN PRESENTATION, ANTITUMOR, INNATE IMMUNITY, NKT CELLS, Text
URL: https://apps.dtic.mil/docs/citations/ADA560605
الإتاحة: Open access content. Open access content
Approved for public release; distribution is unlimited.
ملاحظة: text/html
English
أرقام أخرى: DTICE ADA560605
832137545
المصدر المساهم: From OAIster®, provided by the OCLC Cooperative.
رقم الأكسشن: edsoai.ocn832137545
قاعدة البيانات: OAIster