Tidal Dwarf Galaxies at Intermediate Redshifts

We present the first attempt at measuring the production rate of tidal dwarf galaxies (TDGs) and estimating their contribution to the overall dwarf population. Using HST/ACS deep imaging data from GOODS and GEMS surveys in conjunction with photometric redshifts from COMBO-17 survey, we performed a morphological analysis for a sample of merging/interacting galaxies in the Extended Chandra Deep Field South and identified tidal dwarf candidates in the rest-frame optical bands. We estimated a production rate about 1.4 {\times} 10^{-5} per Gyr per comoving volume for long-lived TDGs with stellar mass 3 {\times} 10^{8-9} solar mass at 0.5<z<1.1. Together with galaxy merger rates and TDG survival rate from the literature, our results suggest that only a marginal fraction (less than 10%) of dwarf galaxies in the local universe could be tidally-originated. TDGs in our sample are on average bluer than their host galaxies in the optical. Stellar population modelling of optical to near-infrared spectral energy distributions (SEDs) for two TDGs favors a burst component with age 400/200 Myr and stellar mass 40%/26% of the total, indicating that a young stellar population newly formed in TDGs. This is consistent with the episodic star formation histories found for nearby TDGs.Comment: 9 pages, 5 figures, Accepted for publication in Astrophysics & Space Scienc

Cutaneous barrier leakage and gut inflammation drive skin disease in Omenn syndrome

Background: Severe early-onset erythroderma and gut inflammation, with massive tissue infiltration of oligoclonal activated T cells are the hallmark of Omenn syndrome (OS). Objective: The impact of altered gut homeostasis in the cutaneous manifestations of OS remains to be clarified. Methods: We analyzed a cohort of 15 patients with OS and the 129Sv/C57BL/6 knock-in Rag2R229Q/R229Q (Rag2R229Q) mouse model. Homing phenotypes of circulating lymphocytes were analyzed by flow cytometry. Inflammatory cytokines and chemokines were examined in the sera by ELISA and in skin biopsies by immunohistochemistry and in situ RNA hybridization. Experimental colitis was induced in mice by dextran sulfate sodium salt. Results: We show that memory/activated T cells from patients with OS and from the Rag2R229Q mouse model of OS abundantly express the skin homing receptors cutaneous lymphocyte associated antigen and CCR4 (Ccr4), associated with high levels of chemokine C-C motif ligands 17 and 22. Serum levels of LPS are also elevated. A broad TH1/TH2/TH17 inflammatory signature is detected in the periphery and in the skin. Increased Tlr4 expression in the skin of Rag2R229Q mice is associated with enhanced cutaneous inflammation on local and systemic administration of LPS. Likewise, boosting colitis in Rag2R229Q mice results in increased frequency of Ccr4+ splenic T cells and worsening of skin inflammation, as indicated by epidermal thickening, enhanced epithelial cell activation, and dermal infiltration by TH1 effector T cells. Conclusions: These results support the existence of an interplay between gut and skin that can sustain skin inflammation in OS