Stellar feedback in a clumpy galaxy at z ∼ 3.4

Giant star-forming regions (clumps) are widespread features of galaxies at z ≈ 1−4. Theory predicts that they can play a crucial role in galaxy evolution, if they survive to stellar feedback for >50 Myr. Numerical simulations show that clumps’ survival depends on the stellar feedback recipes that are adopted. Up to date, observational constraints on both clumps’ outflows strength and gas removal time-scale are still uncertain. In this context, we study a line-emitting galaxy at redshift z ≃ 3.4 lensed by the foreground galaxy cluster Abell 2895. Four compact clumps with sizes ≲280 pc and representative of the low-mass end of clumps’ mass distribution (stellar masses ≲2 × 108 M⊙) dominate the galaxy morphology. The clumps are likely forming stars in a starbursting mode and have a young stellar population (∼10 Myr). The properties of the Lyman-α (Lyα) emission and nebular far-ultraviolet absorption lines indicate the presence of ejected material with global outflowing velocities of ∼200–300 km s−1. Assuming that the detected outflows are the consequence of star formation feedback, we infer an average mass loading factor (η) for the clumps of ∼1.8–2.4 consistent with results obtained from hydrodynamical simulations of clumpy galaxies that assume relatively strong stellar feedback. Assuming no gas inflows (semiclosed box model), the estimates of η suggest that the time-scale over which the outflows expel the molecular gas reservoir (≃7 × 108 M⊙) of the four detected low-mass clumps is ≲50 Myr

PLoS Pathog

Cytomegalovirus (CMV) is a leading infectious cause of morbidity in immune-compromised patients. γδ T cells have been involved in the response to CMV but their role in protection has not been firmly established and their dependency on other lymphocytes has not been addressed. Using C57BL/6 αβ and/or γδ T cell-deficient mice, we here show that γδ T cells are as competent as αβ T cells to protect mice from CMV-induced death. γδ T cell-mediated protection involved control of viral load and prevented organ damage. γδ T cell recovery by bone marrow transplant or adoptive transfer experiments rescued CD3ε-/- mice from CMV-induced death confirming the protective antiviral role of γδ T cells. As observed in humans, different γδ T cell subsets were induced upon CMV challenge, which differentiated into effector memory cells. This response was observed in the liver and lungs and implicated both CD27+ and CD27- γδ T cells. NK cells were the largely preponderant producers of IFNγ and cytotoxic granules throughout the infection, suggesting that the protective role of γδ T cells did not principally rely on either of these two functions. Finally, γδ T cells were strikingly sufficient to fully protect Rag-/-γc-/- mice from death, demonstrating that they can act in the absence of B and NK cells. Altogether our results uncover an autonomous protective antiviral function of γδ T cells, and open new perspectives for the characterization of a non classical mode of action which should foster the design of new γδ T cell based therapies, especially useful in αβ T cell compromised patients

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