التفاصيل البيبلوغرافية
| العنوان: |
Deficiency of iPLA2β Primes Immune Cells for Proinflammation: Potential Involvement in Age-Related Mesenteric Lymph Node Lymphoma |
| المؤلفون: |
Johannes Inhoffen, Sabine Tuma-Kellner, Beate Straub, Wolfgang Stremmel, Walee Chamulitrat |
| المصدر: |
Cancers; Volume 7; Issue 4; Pages: 2427-2442 |
| بيانات النشر: |
Multidisciplinary Digital Publishing Institute |
| سنة النشر: |
2015 |
| المجموعة: |
MDPI Open Access Publishing |
| مصطلحات موضوعية: |
Kupffer cells, lymphocytes, immune response, PLA2G6, CD95/FasL, M1 and Th1 cytokines, mesenteric lymph node lymphoma |
| الوصف: |
Proinflammation can predispose the body to autoimmunity and cancer. We have reported that iPLA2β−/− mice are susceptible to autoimmune hepatitis and colitis. Here we determined whether cytokine release by immune cells could be affected by iPLA2β deficiency alone or combined with CD95/FasL-antibody treatment in vivo. We also determined whether cancer risk could be increased in aged mutant mice. Immune cells were isolated from 3-month old male WT and iPLA2β−/− mice, and some were injected with anti-CD95/FasL antibody for 6 h. Kupffer cells (KC) or splenocytes and liver lymphocytes were stimulated in vitro by lipopolysaccharide or concanavalinA, respectively. Whole-body iPLA2β deficiency caused increased apoptosis in liver, spleen, and mesenteric lymph node (MLN). KC from mutant mice showed suppressed release of TNFα and IL-6, while their splenocytes secreted increased levels of IFNγ and IL-17a. Upon CD95/FasL activation, the mutant KC in turn showed exaggerated cytokine release, this was accompanied by an increased release of IFNγ and IL-17a by liver lymphocytes. Aged iPLA2β−/− mice did not show follicular MLN lymphoma commonly seen in aged C57/BL6 mice. Thus, iPLA2β deficiency renders M1- and Th1/Th17-proinflammation potentially leading to a reduction in age-related MLN lymphoma during aging. |
| نوع الوثيقة: |
text |
| وصف الملف: |
application/pdf |
| اللغة: |
English |
| Relation: |
https://dx.doi.org/10.3390/cancers7040901 |
| DOI: |
10.3390/cancers7040901 |
| الاتاحة: |
https://doi.org/10.3390/cancers7040901 |
| Rights: |
https://creativecommons.org/licenses/by/4.0/ |
| رقم الانضمام: |
edsbas.AF99E865 |
| قاعدة البيانات: |
BASE |