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Deficiency of iPLA(2)β Primes Immune Cells for Proinflammation: Potential Involvement in Age-Related Mesenteric Lymph Node Lymphoma
Proinflammation can predispose the body to autoimmunity and cancer. We have reported that iPLA(2)β(−/−) mice are susceptible to autoimmune hepatitis and colitis. Here we determined whether cytokine release by immune cells could be affected by iPLA(2)β deficiency alone or combined with CD95/FasL-anti...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4695901/ https://www.ncbi.nlm.nih.gov/pubmed/26690222 http://dx.doi.org/10.3390/cancers7040901 |
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author | Inhoffen, Johannes Tuma-Kellner, Sabine Straub, Beate Stremmel, Wolfgang Chamulitrat, Walee |
author_facet | Inhoffen, Johannes Tuma-Kellner, Sabine Straub, Beate Stremmel, Wolfgang Chamulitrat, Walee |
author_sort | Inhoffen, Johannes |
collection | PubMed |
description | Proinflammation can predispose the body to autoimmunity and cancer. We have reported that iPLA(2)β(−/−) mice are susceptible to autoimmune hepatitis and colitis. Here we determined whether cytokine release by immune cells could be affected by iPLA(2)β 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 iPLA(2)β(−/−) 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 iPLA(2)β 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 iPLA(2)β(−/−) mice did not show follicular MLN lymphoma commonly seen in aged C57/BL6 mice. Thus, iPLA(2)β deficiency renders M1- and Th1/Th17-proinflammation potentially leading to a reduction in age-related MLN lymphoma during aging. |
format | Online Article Text |
id | pubmed-4695901 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-46959012016-01-19 Deficiency of iPLA(2)β Primes Immune Cells for Proinflammation: Potential Involvement in Age-Related Mesenteric Lymph Node Lymphoma Inhoffen, Johannes Tuma-Kellner, Sabine Straub, Beate Stremmel, Wolfgang Chamulitrat, Walee Cancers (Basel) Article Proinflammation can predispose the body to autoimmunity and cancer. We have reported that iPLA(2)β(−/−) mice are susceptible to autoimmune hepatitis and colitis. Here we determined whether cytokine release by immune cells could be affected by iPLA(2)β 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 iPLA(2)β(−/−) 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 iPLA(2)β 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 iPLA(2)β(−/−) mice did not show follicular MLN lymphoma commonly seen in aged C57/BL6 mice. Thus, iPLA(2)β deficiency renders M1- and Th1/Th17-proinflammation potentially leading to a reduction in age-related MLN lymphoma during aging. MDPI 2015-12-09 /pmc/articles/PMC4695901/ /pubmed/26690222 http://dx.doi.org/10.3390/cancers7040901 Text en © 2015 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons by Attribution (CC-BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Inhoffen, Johannes Tuma-Kellner, Sabine Straub, Beate Stremmel, Wolfgang Chamulitrat, Walee Deficiency of iPLA(2)β Primes Immune Cells for Proinflammation: Potential Involvement in Age-Related Mesenteric Lymph Node Lymphoma |
title | Deficiency of iPLA(2)β Primes Immune Cells for Proinflammation: Potential Involvement in Age-Related Mesenteric Lymph Node Lymphoma |
title_full | Deficiency of iPLA(2)β Primes Immune Cells for Proinflammation: Potential Involvement in Age-Related Mesenteric Lymph Node Lymphoma |
title_fullStr | Deficiency of iPLA(2)β Primes Immune Cells for Proinflammation: Potential Involvement in Age-Related Mesenteric Lymph Node Lymphoma |
title_full_unstemmed | Deficiency of iPLA(2)β Primes Immune Cells for Proinflammation: Potential Involvement in Age-Related Mesenteric Lymph Node Lymphoma |
title_short | Deficiency of iPLA(2)β Primes Immune Cells for Proinflammation: Potential Involvement in Age-Related Mesenteric Lymph Node Lymphoma |
title_sort | deficiency of ipla(2)β primes immune cells for proinflammation: potential involvement in age-related mesenteric lymph node lymphoma |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4695901/ https://www.ncbi.nlm.nih.gov/pubmed/26690222 http://dx.doi.org/10.3390/cancers7040901 |
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