Deficiency of iPLA₂β Primes Immune Cells for Proinflammation: Potential Involvement in Age-Related Mesenteric Lymph Node Lymphoma.

ABSTRACT: 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 show

SUBMITTER: Inhoffen J 

PROVIDER: S-EPMC4695901 | biostudies-literature | 2015 Dec

REPOSITORIES: biostudies-literature