In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

[EX Q]: Context: Environmental conditions (eg, latitude) play a critical role in the susceptibility and severity of many autoimmune disorders, including multiple sclerosis (MS). Here, we investigated the mechanisms underlying the beneficial effects of immune regulatory processes induced in the skin by moderate ultraviolet B (UVB) radiation on central nervous system (CNS) autoimmunity.', 'Effects of UVB light were analyzed in a murine model of CNS autoimmunity (experimental autoimmune encephalomyelitis). Additionally, patients with relapsing-remitting MS were treated with narrowband UVB phototherapy. Immunomodulatory effects were examined in skin biopsies, serum samples, and immune cells of the peripheral blood.', 'Regulatory T cells (Tregs), which are induced locally in the skin-draining lymph nodes in response to UVB exposure, connect the cutaneous immune response to CNS immunity by migration to the sites of inflammation (blood, spleen, CNS). Here, they attenuate the inflammatory response and ameliorate disease symptoms. Treg-inducing tolerogenic dendritic cells (DCs) were further necessary for induction of this systemic immune regulation by UVB radiation, because ablation of Langerhans cells abolished the UVB-induced phenotype. MS patients treated with UVB phototherapy showed an increase in induced Tregs and tolerogenic DCs accompanied by the downregulation of the T-cell effector cytokine interleukin 21. The treatment further induced elevated serum levels of vitamin D.\Question: Does ultraviolet B light attenuate the systemic immune response in central nervous system autoimmunity?
[EX A]: Local UVB radiation of the skin influences systemic immune reactions and attenuates systemic autoimmunity via the induction of skin-derived tolerogenic DCs and Tregs. Our data could have implications for the understanding or therapeutic modulation of environmental factors that influence immune tolerance.

[EX Q]: Context: To find permanent prostate implant (PPI) pre-plan dosimetric parameters that predict post-implant D90 ≥ 140 Gy.', 'Pre-plans were evaluated for 504 patients undergoing PPI with (125)I seeds for low or intermediate risk prostate cancer. Baseline patient and disease factors, numbers of seeds, ratios of number of seeds to available positions (occupancy proportion), and distances between the 100% isodose line and edge of the prostate (margin) planned for the whole prostate (WP), superior (S), inferior (I), anterior (A), and posterior (P) halves, SA, SP, IA, and IP quarters, and superior (ST), inferior (IT), and middle (MT) thirds, and anterior (AT) and posterior (PT) middle one-sixth segments were analyzed by post-implant D90 subset (≥ 140 Gy vs. < 140 Gy).', '20% had post-implant D90 < 140 Gy (mean: 128.0 Gy, range: 97.5-139.2) vs. ≥ 140 Gy (mean: 154.4 Gy, range: 140.0-193.5). The D90 ≥ 140 Gy subset had larger AT and IA segment mean numbers of seeds (p = 0.01, 0.046), larger WP, S, A, SA, ST, AT, and MT segment mean margins (p = 0.01, 0.01, 0.001, 0.0001, 0.03, 0.005, 0.02), and lower PT segment occupancy proportion (p = 0.004). On multivariate analysis, independent predictors of post-implant D90 ≥ 140 Gy were increased SA mean margin, no pre-implant 5-α-reductase inhibitor, higher pre-plan D90, decreased P occupancy proportion, no pre-implant hormone therapy, and decreased SP mean margin.\Question: Do pre-plan parameters predict post-implant D90 ≥ 140 Gy for ( 125 ) I permanent prostate implants?
[EX A]: Higher occupancy proportion and larger margins anteriorly and reduced occupancy proportion, and smaller margins posteriorly on PPI pre-plans predict post-implant D90 ≥ 140 Gy.

[EX Q]: Context: Infection with Helicobacter pylori is the strongest known risk factor for adenocarcinoma of the stomach. Tumorigenic transformation of gastric epithelium induced by H. pylori is a highly complex process driven by an active interplay between bacterial virulence and host factors, many aspects of which remain obscure. In this work, we investigated the degradation of p53 tumour suppressor induced by H. pylori.', 'Expression of p53 protein in gastric biopsies was assessed by immunohistochemistry. Gastric cells were co-cultured with H. pylori strains isolated from high-gastric risk and low-gastric risk areas and assessed for expression of p53, p14ARF and cytotoxin-associated gene A (CagA) by immunoblotting. siRNA was used to inhibit activities of ARF-BP1 and Human Double Minute 2 (HDM2) proteins.', 'Our analysis demonstrated that H. pylori strains expressing high levels of CagA virulence factor and associated with a higher gastric cancer risk more strongly suppress p53 compared with low-risk strains in vivo and in vitro. We found that degradation of p53 induced by bacterial CagA protein is mediated by host HDM2 and ARF-BP1 E3 ubiquitin ligases, while the p14ARF protein counteracts H. pylori-induced signalling.\Question: Does bacterial CagA protein induce degradation of p53 protein in a p14ARF-dependent manner?
[EX A]:
Our results provide novel evidence that tumorigenicity associated with H. pylori infection is linked to inhibition of p53 protein by CagA. We propose a model in which CagA-induced degradation of p53 protein is determined by a relative level of p14ARF. In cells in which p14ARF levels were decreased due to hypermethylation or deletion of the p14ARF gene, H. pylori efficiently degraded p53, whereas p53 is protected in cells expressing high levels of p14ARF.