In this task, you are given an abstract of article. Your task is to generate title for this article. Preferred titles are under thirty words.

Example Input: To efficiently counteract pathogens, plants rely on a complex set of immune responses that are tightly regulated to allow the timely activation, appropriate duration and adequate amplitude of defense programs. The coordination of the plant immune response is known to require the activity of the ubiquitin/proteasome system, which controls the stability of proteins in eukaryotes. Here, we demonstrate that the N-end rule pathway, a subset of the ubiquitin/proteasome system, regulates the defense against a wide range of bacterial and fungal pathogens in the model plant Arabidopsis thaliana. We show that this pathway positively regulates the biosynthesis of plant-defense metabolites such as glucosinolates, as well as the biosynthesis and response to the phytohormone jasmonic acid, which plays a key role in plant immunity. Our results also suggest that the arginylation branch of the N-end rule pathway regulates the timing and amplitude of the defense program against the model pathogen Pseudomonas syringae AvrRpm1.
Example Output: The N-end rule pathway regulates pathogen responses in plants.

Example Input: CD8(+) T cells can respond to unrelated infections in an Ag-independent manner. This rapid innate-like immune response allows Ag-experienced T cells to alert other immune cell types to pathogenic intruders. In this study, we show that murine CD8(+) T cells can sense TLR2 and TLR7 ligands, resulting in rapid production of IFN- but not of TNF- and IL-2. Importantly, Ag-experienced T cells activated by TLR ligands produce sufficient IFN- to augment the activation of macrophages. In contrast to Ag-specific reactivation, TLR-dependent production of IFN- by CD8(+) T cells relies exclusively on newly synthesized transcripts without inducing mRNA stability. Furthermore, transcription of IFN- upon TLR triggering depends on the activation of PI3K and serine-threonine kinase Akt, and protein synthesis relies on the activation of the mechanistic target of rapamycin. We next investigated which energy source drives the TLR-induced production of IFN-. Although Ag-specific cytokine production requires a glycolytic switch for optimal cytokine release, glucose availability does not alter the rate of IFN- production upon TLR-mediated activation. Rather, mitochondrial respiration provides sufficient energy for TLR-induced IFN- production. To our knowledge, this is the first report describing that TLR-mediated bystander activation elicits a helper phenotype of CD8(+) T cells. It induces a short boost of IFN- production that leads to a significant but limited activation of Ag-experienced CD8(+) T cells. This activation suffices to prime macrophages but keeps T cell responses limited to unrelated infections.
Example Output: TLR-Mediated Innate Production of IFN- by CD8+ T Cells Is Independent of Glycolysis.

Example Input: Porphyria cutanea tarda (PCT) can occur in HIV patients. Current evidence suggests that HIV infection may interfere with the hepatic cytochrome oxidase system, leading to porphyrin metabolism impairment. Moreover, chronic hemodialysis in renal failure may be a risk factor for PCT. In addition to the contributory factors for PCT associated to HIV infection, it is possible that porphyrin accumulation secondary to renal failure may play a role in the expression of this disease. We report a case of PCT in an HIV-1 infected patient under blood dialysis, refractory to antimalarials and controlled with desferrioxamine.
Example Output:
Desferrioxamine treatment of porphyria cutanea tarda in a patient with HIV and chronic renal failure.