Active Galactic Nuclei and the Truncation of Star Formation in K+A Galaxies

We have searched for active galactic nuclei (AGNs) in K+A galaxies, using multiwavelength imaging and spectroscopy in the Bootes field of the NOAO Deep Wide-Field Survey. The K+A galaxies, which have had their star formation rapidly truncated, are selected via their strong Balmer absorption lines and weak H-alpha emission. Our sample consists of 24 K+A galaxies selected from 6594 0.10<z<0.35 galaxies brighter than I=20 with optical spectroscopy from the AGN and Galaxy Evolution Survey. Two thirds of the K+A galaxies are likely ongoing galaxy mergers, with nearby companion galaxies or tidal tails. Galaxy mergers may be responsible for the truncation of star formation, or we are observing the aftermath of merger triggered starbursts. As expected, the optical colors of K+A galaxies largely fall between blue galaxies with ongoing star formation and red passive galaxies. However, only 1% of the galaxies with colors between the red and blue populations are K+A galaxies, and we conclude that the truncation of star formation in K+A galaxies must have been unusually abrupt (<100 Myr). We examined the AGN content of K+A galaxies with both optical emission-line ratios (BPT diagrams) and Chandra X-ray imaging. At least half of all K+A galaxies display the optical emission-line ratios of AGNs, and a third of M_R<-22 K+A galaxies host AGNs with X-ray luminosities of 10^{42} erg/s. The faintest K+A galaxies do not show clear evidence for hosting AGNs, having emission-line ratios consistent with photoionization by massive stars and few X-ray detections. We speculate that two mechanisms may be responsible for the truncation of star formation in K+A galaxies, with AGN feedback only playing a role in M_R<-20.5 galaxies.Comment: Accepted for publication in the Astrophysical Journal. 13 pages, 8 figure

Possible role of human herpesvirus 8 in the lymphoproliferative disorders in common variable immunodeficiency

Patients who have common variable immunodeficiency (CVID) and granulomatous/lymphocytic interstitial lung disease (GLILD) are at high risk for early mortality and B cell lymphomas. Infection with human herpes virus type 8 (HHV8), a B cell lymphotrophic virus, is linked to lymphoproliferative disorders in people who have secondary immunodeficiencies. Therefore, we determined the prevalence of HHV8 infection in CVID patients with GLILD. Genomic DNA isolated from peripheral blood mononuclear cells was screened by nested- and real time-quantitative PCR (QRT-PCR) for the presence of HHV8 genome. It was positive in 6/9 CVID patients with GLILD (CVID-GLILD), 1/21 CVID patients without GLILD (CVID-control), and no patients receiving intravenous gamma globulin (n = 13) or normal blood donors (n = 20). Immunohistochemistry (IHC) demonstrated expression of the latency-associated nuclear antigen-1 (LANA-1) in the biopsies of the lung, liver, and bone marrow of four patients with CVID-GLILD. One CVID-GLILD patient developed a B cell lymphoma during the course of the study. QRT-PCR demonstrated high copy number of HHV8 genome and IHC showed diffuse staining for LANA-1 in the malignant lymph node. HHV8 infection may be an important factor in the pathogenesis of the interstitial lung disease and lymphoproliferative disorders in patients with CVID

Identification of a Cytotoxic Form of Dimeric Interleukin-2 in Murine Tissues

Interleukin-2 (IL-2) is a multi-faceted cytokine, known for promoting proliferation, survival, and cell death depending on the cell type and state. For example, IL-2 facilitates cell death only in activated T cells when antigen and IL-2 are abundant. The availability of IL-2 clearly impacts this process. Our laboratory recently demonstrated that IL-2 is retained in blood vessels by heparan sulfate, and that biologically active IL-2 is released from vessel tissue by heparanase. We now demonstrate that heparanase digestion also releases a dimeric form of IL-2 that is highly cytotoxic to cells expressing the IL-2 receptor. These cells include “traditional” IL-2 receptor-bearing cells such as lymphocytes, as well as those less well known for IL-2 receptor expression, such as epithelial and smooth muscle cells. The morphologic changes and rapid cell death induced by dimeric IL-2 imply that cell death is mediated by disruption of membrane permeability and subsequent necrosis. These findings suggest that IL-2 has a direct and unexpectedly broad influence on cellular homeostatic mechanisms in both immune and non-immune systems