A tale of two feedbacks: star formation in the host galaxies of radio AGNs

Several lines of argument support the existence of a link between activity at the nuclei of galaxies, in the form of an accreting supermassive black hole, and star formation activity in these galaxies. Radio jets have long been argued to be an ideal mechanism that allows active galactic nuclei (AGNs) to interact with their host galaxies and affect star formation. We use a sample of radio sources in the North Ecliptic Pole (NEP) field to study the nature of this putative link, by means of spectral energy distribution (SED) fitting. We employ the excellent spectral coverage of the AKARI infrared space telescope and the rich ancillary data available in the NEP to build SEDs extending from UV to far-IR wavelengths. We find a significant AGN component in our sample of relatively faint radio sources (<mJy). A positive correlation is found between the luminosity of the AGN component and that of star formation in the host galaxy, independent of the radio luminosity. In contrast, for narrow redshift and AGN luminosity ranges, we find that increasing radio luminosity leads to a decrease in the specific star formation rate. The most radio-loud AGNs are found to lie on the main sequence of star formation for their respective redshifts. For the first time, we potentially see such a two-sided feedback process in the same sample. We discuss the possible suppression of star formation, but not total quenching, in systems with strong radio jets, that supports the maintenance nature of feedback from radio AGN jets

Activation of ERα Signaling Differentially Modulates IFN-γ Induced HLA-Class II Expression in Breast Cancer Cells

The coordinate regulation of HLA class II (HLA-II) is controlled by the class II transactivator, CIITA, and is crucial for the development of anti-tumor immunity. HLA-II in breast carcinoma is associated with increased IFN-γ levels, reduced expression of the estrogen receptor (ER) and reduced age at diagnosis. Here, we tested the hypothesis that estradiol (E2) and ERα signaling contribute to the regulation of IFN-γ inducible HLA-II in breast cancer cells. Using a panel of established ER− and ER+ breast cancer cell lines, we showed that E2 attenuated HLA-DR in two ER+ lines (MCF-7 and BT-474), but not in T47D, while it augmented expression in ER− lines, SK-BR-3 and MDA-MB-231. To further study the mechanism(s), we used paired transfectants: ERα+ MC2 (MDA-MB-231 c10A transfected with the wild type ERα gene) and ERα− VC5 (MDA-MB-231 c10A transfected with the empty vector), treated or not with E2 and IFN-γ. HLA-II and CIITA were severely reduced in MC2 compared to VC5 and were further exacerbated by E2 treatment. Reduced expression occurred at the level of the IFN-γ inducible CIITA promoter IV. The anti-estrogen ICI 182,780 and gene silencing with ESR1 siRNA reversed the E2 inhibitory effects, signifying an antagonistic role for activated ERα on CIITA pIV activity. Moreover, STAT1 signaling, necessary for CIITA pIV activation, and selected STAT1 regulated genes were variably downregulated by E2 in transfected and endogenous ERα positive breast cancer cells, whereas STAT1 signaling was noticeably augmented in ERα− breast cancer cells. Collectively, these results imply immune escape mechanisms in ERα+ breast cancer may be facilitated through an ERα suppressive mechanism on IFN-γ signaling