bluuebunny/crossref_metadata_2025_split huggingface dataset:
Isolation and characterization of EST‐SSR markers in Schima mertensiana (Theaceae) using pyrosequencing technology
Authors: Setsuko Suzuki , Uchiyama Kentaro , Sugai Kyoko , Yoshimaru Hiroshi 
Published: December 2011

• Premise of the study: Microsatellite or simple sequence repeat (SSR) markers from expressed sequence tags (ESTs) in Schima mertensiana, an evergreen tree that is endemic to the Bonin Islands, were developed to facilitate evaluation of the species's population genetic structure.• Methods and Results: Using 149831 ESTs derived by pyrosequencing S. mertensiana complementary DNA (cDNA), 683 EST‐SSRs were developed, 48 of which were tested for amplification. Thirty of the 48 showed clear amplification and detected polymorphism in sampled populations, with mean expected heterozygosity at the amplified loci ranging from 0.045 to 0.874 (average 0.545).• Conclusions: The markers developed in this study can be used for future studies of the genetic structure of S. mertensiana and related species.
The cuticle on the gametophyte calyptra matures before the sporophyte cuticle in the moss Funaria hygrometrica (Funariaceae)
Authors: Budke Jessica M. , Goffinet Bernard , Jones Cynthia S. 
Published: December 2011

• Premise of the study: In vascular plants, leaf primordia prevent desiccation of the shoot apical meristem. Lacking leaves, the undifferentiated moss sporophyte apex is covered by the calyptra, a cap of maternal gametophyte tissue that is hypothesized to function in desiccation protection. Herein, we compare cuticle development on the calyptra and sporophyte to assess the calyptra's potential to protect the sporophyte from desiccation. As the first comprehensive study of moss sporophyte cuticle development, this research broadens our perspectives on cuticle development and evolution across embryophytes.• Methods: Calyptrae and sporophytes at nine developmental stages were collected from a laboratory‐grown population of the moss Funaria hygrometrica. Tissues were embedded, sectioned, then examined using transmission electron microscopy. Epidermal cells were measured for thickness of the cuticle layers, cell wall thickness, and lumen size.• Key results: The calyptra cuticle develops precociously and reaches maturity before the sporophyte cuticle. Calyptrae are covered by a four‐layered cuticle at all stages, whereas sporophyte cuticle maturation is delayed until sporangium formation. The development and thickening of the sporophyte cuticle occurs in an acropetal wave.• Conclusions: A multilayered calyptra cuticle at the earliest developmental stages is consistent with its ability to protect the immature sporophyte from desiccation. Young sporophytes lack a complex cuticle and thus may require protection, whereas in older sporophytes a mature cuticle develops. The moss calyptra is not a vestigial structure, but rather the calyptra's role in preventing desiccation offers a functional explanation for calyptra retention during the 450 Myr of moss evolution.
A new Oligocene Calocedrus from South China and its implications for transpacific floristic exchanges
Authors: Shi Gongle , Zhou Zhiyan , Xie Zhiming 
Published: January 2012

• Premise of the Study: Calocedrus is among the genera with a typical eastern Asian–western North American disjunct distribution today. The origin of its modern distribution pattern can be better understood by examining its fossil record.• Methods: The present article reports for the first time a new fossil species of this genus based on compressed material from the Oligocene Ningming Formation of Guangxi, South China, in its present major distribution area in eastern Asia.• Key Results: Calocedrus huashanensis sp. nov. is most similar to the two extant eastern Asian species, C. macrolepis and C. formosana, in gross morphology of foliage shoots and bears a close resemblance to the latter in cuticle structure. It shows a general similarity to the North American fossil representatives of the genus in alternately branched foliage shoots but is clearly different from the European Paleogene species characterized by oppositely branched leafy shoots.• Conclusions: This discovery provides new evidence for the floristic exchange of this genus between eastern Asia and North America before the Oligocene (most likely in the Eocene), presumably via the Bering land bridge. The flattened leafy shoots and dimorphic leaves with thin cuticle, open stomatal pits, and shallowly sunken guard cells of the present fossils suggest a rather humid climate during the Oligocene in the Ningming area, South China.
Anatomical, biochemical, and photosynthetic responses to recent allopolyploidy in Glycine dolichocarpa (Fabaceae)
Authors: Coate Jeremy E. , Luciano Amelia K. , Seralathan Vasu , Minchew Kevin J. , Owens Tom G. , Doyle Jeff J. 
Published: December 2011

• Premise of the study: Previous studies have shown that polyploidy has pronounced effects on photosynthesis. Most of these studies have focused on synthetic or recently formed autopolyploids, and comparatively little is known about the integrated effects of natural allopolyploidy, which involves hybridity and genome doubling and often incorporates multiple genotypes through recurrent origins and lineage recombination.• Methods: Glycine dolichocarpa (designated T2) is a natural allotetraploid with multiple origins. We quantified 21 anatomical, biochemical, and physiological phenotypes relating to photosynthesis in T2 and its diploid progenitors, G. tomentella (D3) and G. syndetika (D4). To assess how direction of cross affects these phenotypes, we included three T2 accessions having D3‐like plastids (T2D3) and two accessions having D4‐like plastids (T2D4).• Key results: T2 accessions were transgressive (more extreme than any diploid accession) for 17 of 21 phenotypes, and species means differed significantly in T2 vs. both progenitors for four of 21 phenotypes (higher for guard cell length, electron transport capacity [Jmax] per palisade cell, and Jmax per mesophyll cell; lower for palisade cells per unit leaf area). Within T2, four of 21 parameters differed significantly between T2D3 and T2D4 (palisade cell volume; chloroplast number and volume per unit leaf area; and Jmax per unit leaf area).• Conclusions: T2 is characterized by transgressive photosynthesis‐related phenotypes (including an ca. 2‐fold increase in Jmax per cell), as well as by significant intraspecies variation correlating with plastid type. These data indicate prominent roles for both nucleotypic effects and cytoplasmic factors in photosynthetic responses to allopolyploidy.
Epidermal Cadm1 Expression Promotes Autoimmune Alopecia via Enhanced T Cell Adhesion and Cytotoxicity
Authors: Giangreco Adam , Hoste Esther , Takai Yoshimi , Rosewell Ian , Watt Fiona M. 
Published: December 2011

Abstract
Autoimmune alopecia is characterized by an extensive epidermal T cell infiltrate that mediates hair follicle destruction. We have investigated the role of cell adhesion molecule 1 (Cadm1; Necl2) in this disease. Cadm1 is expressed by epidermal cells and mediates heterotypic adhesion to lymphocytes expressing class 1-restricted T cell-associated molecule (CRTAM). Using a murine autoimmune alopecia model, we observed an increase in early-activated cytotoxic (CD8-restricted, CRTAM-expressing) T cells, which preferentially associated with hair follicle keratinocytes expressing Cadm1. Coculture with Cadm1-transduced MHC-matched APCs stimulated alopecic lymph node cells to release IL-2 and IFN-γ. Overexpression of Cadm1 in cultured human keratinocytes did not promote cytokine secretion, but led to increased adhesion of alopecic cytotoxic T cells and enhanced T cell cytotoxicity in an MHC-independent manner. Epidermal overexpression of Cadm1 in transgenic mice led to increased autoimmune alopecia susceptibility relative to nontransgenic littermate controls. Our findings reveal that Cadm1 expression in the hair follicle plays a role in autoimmune alopecia.
Thy-1 (CD90) Is an Interacting Partner for CD97 on Activated Endothelial Cells
Authors: Wandel Elke , Saalbach Anja , Sittig Doreen , Gebhardt Carl , Aust Gabriela 
Published: December 2011

Abstract
Leukocyte recruitment in response to inflammatory signals is governed, in part, by binding to Thy-1 (CD90) on activated endothelial cells (EC). In this study, we characterized the adhesion G-protein coupled receptor CD97, present on peripheral myeloid cells, as a novel interacting partner for Thy-1. CD97 was upregulated on polymorphonuclear cells (PMNC) of patients with psoriasis. In psoriatic skin lesions, CD97+ myeloid cells colocalized with Thy-1+ EC of small vessels in microabscesses, suggesting an interaction between CD97 and Thy-1 that was further examined by adhesion and protein-binding assays. PMNC and cell lines stably overexpressing CD97 adhered specifically to Thy-1+–activated human dermal EC, Thy-1+ CHO cells, and immobilized Thy-1 protein. Binding of the CD97+ CHO clones correlated with their CD97 expression level. Soluble CD97 bound specifically to immobilized Thy-1 protein, as well as Thy-1+–activated EC and CHO cells. In all assays, cellular adhesion or protein binding was blocked partially by CD97 and Thy-1–blocking mAb. Our data suggested that CD97 interacts via its stalk with Thy-1 because mAb directed to the stalk of CD97 showed stronger blocking compared with mAb to its epidermal growth factor-like domains, and binding was calcium independent. Moreover, soluble CD97 without the stalk and soluble EMR2, containing highly homologous epidermal growth factor-like domains but a different stalk, failed to bind. In summary, binding of leukocytes to activated endothelium mediated by the interaction of CD97 with Thy-1 is involved in firm adhesion of PMNC during inflammation and may play a role in the regulation of leukocyte trafficking to inflammatory sites.
RANKL Induces Organized Lymph Node Growth by Stromal Cell Proliferation
Authors: Hess Estelle , Duheron Vincent , Decossas Marion , Lézot Frédéric , Berdal Ariane , Chea Sylvestre , Golub Rachel , Bosisio Mattéo R. , Bridal S. Lori , Choi Yongwon , Yagita Hideo , Mueller Christopher G. 
Published: December 2011

Abstract
RANK and its ligand RANKL play important roles in the development and regulation of the immune system. We show that mice transgenic for Rank in hair follicles display massive postnatal growth of skin-draining lymph nodes. The proportions of hematopoietic and nonhematopoietic stromal cells and their organization are maintained, with the exception of an increase in B cell follicles. The hematopoietic cells are not activated and respond to immunization by foreign Ag and adjuvant. We demonstrate that soluble RANKL is overproduced from the transgenic hair follicles and that its neutralization normalizes lymph node size, inclusive area, and numbers of B cell follicles. Reticular fibroblastic and vascular stromal cells, important for secondary lymphoid organ formation and organization, express RANK and undergo hyperproliferation, which is abrogated by RANKL neutralization. In addition, they express higher levels of CXCL13 and CCL19 chemokines, as well as MAdCAM-1 and VCAM-1 cell-adhesion molecules. These findings highlight the importance of tissue-derived cues for secondary lymphoid organ homeostasis and identify RANKL as a key molecule for controlling the plasticity of the immune system.
Transient TLR Activation Restores Inflammatory Response and Ability To Control Pulmonary Bacterial Infection in Germfree Mice
Authors: Fagundes Caio T. , Amaral Flávio A. , Vieira Angélica T. , Soares Adriana C. , Pinho Vanessa , Nicoli Jacques R. , Vieira Leda Q. , Teixeira Mauro M. , Souza Danielle G. 
Published: December 2011

Abstract
Mammals are colonized by an astronomical number of commensal microorganisms on their environmental exposed surfaces. These symbiotic species build up a complex community that aids their hosts in several physiological activities. We have shown that lack of intestinal microbiota is accompanied by a state of active IL-10–mediated inflammatory hyporesponsiveness. The present study investigated whether the germfree state and its hyporesponsive phenotype alter host resistance to an infectious bacterial insult. Experiments performed in germfree mice infected with Klebsiella pneumoniae showed that these animals are drastically susceptible to bacterial infection in an IL-10–dependent manner. In germfree mice, IL-10 restrains proinflammatory mediator production and neutrophil recruitment and favors pathogen growth and dissemination. Germfree mice were resistant to LPS treatment. However, priming of these animals with several TLR agonists recovered their inflammatory responsiveness to sterile injury. LPS pretreatment also rendered germfree mice resistant to pulmonary K. pneumoniae infection, abrogated IL-10 production, and restored TNF-α and CXCL1 production and neutrophil mobilization into lungs of infected germfree mice. This effective inflammatory response mounted by LPS-treated germfree mice resulted in bacterial clearance and enhanced survival upon infection. Therefore, host colonization by indigenous microbiota alters the way the host reacts to environmental infectious stimuli, probably through activation of TLR-dependent pathways. Symbiotic gut colonization enables proper inflammatory response to harmful insults to the host, and increases resilience of the entire mammal-microbiota consortium to environmental pressures.
Early Responding Dendritic Cells Direct the Local NK Response To Control Herpes Simplex Virus 1 Infection within the Cornea
Authors: Frank Gregory M. , Buela Kristine-Ann G. , Maker Dawn M. , Harvey Stephen A. K. , Hendricks Robert L. 
Published: December 2011

Abstract
Dendritic cells (DCs) regulate both innate and adaptive immune responses. In this article, we exploit the unique avascularity of the cornea to examine a role for local or very early infiltrating DCs in regulating the migration of blood-derived innate immune cells toward HSV-1 lesions. A single systemic diphtheria toxin treatment 2 d before HSV-1 corneal infection transiently depleted CD11c+ DCs from both the cornea and lymphoid organs of CD11c-DTR bone marrow chimeric mice for up to 24 h postinfection. Transient DC depletion significantly delayed HSV-1 clearance from the cornea through 6 d postinfection. No further compromise of viral clearance was observed when DCs were continuously depleted throughout the first week of infection. DC depletion did not influence extravasation of NK cells, inflammatory monocytes, or neutrophils into the peripheral cornea, but it did significantly reduce migration of NK cells and inflammatory monocytes, but not neutrophils, toward the HSV-1 lesion in the central cornea. Depletion of NK cells resulted in similar loss of viral control to transient DC ablation. Our findings demonstrate that resident corneal DCs and/or those that infiltrate the cornea during the first 24 h after HSV-1 infection contribute to the migration of NK cells and inflammatory monocytes into the central cornea, and are consistent with a role for NK cells and possibly inflammatory monocytes, but not polymorphonuclear neutrophils, in clearing HSV-1 from the infected cornea.
TLR2 Activation Enhances HIV Nuclear Import and Infection through T Cell Activation-Independent and -Dependent Pathways
Authors: Ding Jian , Chang Theresa L. 
Published: December 2011

Abstract
TLR2 activation plays a crucial role in Neisseria gonorrheae-mediated enhancement of HIV infection of resting CD4+ T cells. We examined signaling pathways involved in the HIV enhancing effect of TLR2. TLR2 but not IL-2 signals promoted HIV nuclear import; however, both signals were required for the maximal enhancing effect. Although TLR2 signaling could not activate T cells, it increased IL-2–induced T cell activation. Cyclosporin A and IkBα inhibitor blocked TLR2-mediated enhancement of HIV infection/nuclear import. PI3K inhibitor blocked HIV infection/nuclear import and T cell activation and exerted a moderate inhibitory effect on cell cycle progression in CD4+ T cells activated by TLR2/IL-2. Blockade of p38 signaling suppressed TLR2-mediated enhancement of HIV nuclear import/infection. However, the p38 inhibitor did not have a significant effect on T cell activation or TCR/CD3-mediated enhancement of HIV infection/nuclear import. The cell cycle arresting reagent aphidicolin blocked TLR2- and TCR/CD3-induced HIV infection/nuclear import. Finally, cyclosporin A and IκBα and PI3K inhibitors but not the p38 inhibitor blocked TLR2-mediated IκBα phosphorylation. Our results suggest that TLR2 activation enhances HIV infection/nuclear import in resting CD4+ T cells through both T cell activation-dependent and -independent mechanisms.
IL-13 Regulates Th17 Secretion of IL-17A in an IL-10–Dependent Manner
Authors: Newcomb Dawn C. , Boswell Madison G. , Huckabee Matthew M. , Goleniewska Kasia , Dulek Daniel E. , Reiss Sara , Lukacs Nicholas W. , Kolls Jay K. , Peebles R. Stokes 
Published: December 2011

Abstract
IL-13 is a central mediator of airway hyperresponsiveness and mucus expression, both hallmarks of asthma. IL-13 is found in the sputum of patients with asthma; therefore, IL-13 is an attractive drug target for treating asthma. We have shown previously that IL-13 inhibits Th17 cell production of IL-17A and IL-21 in vitro. Th17 cells are associated with autoimmune diseases, host immune responses, and severe asthma. In this study, we extend our in vitro findings and determine that IL-13 increases IL-10 production from Th17-polarized cells and that IL-13–induced IL-10 production negatively regulates the secretion of IL-17A and IL-21. To determine if IL-13 negatively regulates lung IL-17A expression via an IL-10–dependent mechanism in vivo, we used a model of respiratory syncytial virus (RSV) strain A2 infection in STAT1 knockout (KO) mice that increases lung IL-17A and IL-13 expression, cytokines not produced during RSV infection in wild-type mice. To test the hypothesis that IL-13 negatively regulates lung IL-17A expression, we created STAT1/IL-13 double KO (DKO) mice. We found that RSV-infected STAT1/IL-13 DKO mice had significantly greater lung IL-17A expression compared with that of STAT1 KO mice and that increased IL-17A expression was abrogated by anti-IL-10 Ab treatment. RSV-infected STAT1/IL-13 DKO mice also had increased neutrophil infiltration compared with that of RSV-infected STAT1 KO mice. Neutralizing IL-10 increased the infiltration of inflammatory cells into the lungs of STAT1 KO mice but not STAT1/IL-13 DKO mice. These findings are vital to understanding the potential side effects of therapeutics targeting IL-13. Inhibiting IL-13 may decrease IL-10 production and increase IL-17A production, thus potentiating IL-17A–associated diseases.
Regulation of Eosinophil Trafficking by SWAP-70 and Its Role in Allergic Airway Inflammation
Authors: Bahaie Nooshin S. , Hosseinkhani M. Reza , Ge Xiao Na , Kang Bit Na , Ha Sung Gil , Blumenthal Malcolm S. , Jessberger Rolf , Rao Savita P. , Sriramarao P. 
Published: December 2011

Abstract
Eosinophils are the predominant inflammatory cells recruited to allergic airways. In this article, we show that human and murine eosinophils express SWAP-70, an intracellular RAC-binding signaling protein, and examine its role in mediating eosinophil trafficking and pulmonary recruitment in a murine model of allergic airway inflammation. Compared with wild-type eosinophils, SWAP-70–deficient (Swap-70−/−) eosinophils revealed altered adhesive interactions within inflamed postcapillary venules under conditions of blood flow by intravital microscopy, exhibiting enhanced slow rolling but decreased firm adhesion. In static adhesion assays, Swap-70−/− eosinophils adhered poorly to VCAM-1 and ICAM-1 and exhibited inefficient leading edge and uropod formation. Adherent Swap-70−/− eosinophils failed to translocate RAC1 to leading edges and displayed aberrant cell surface localization/distribution of α4 and Mac-1. Chemokine-induced migration of Swap-70−/− eosinophils was significantly decreased, correlating with reduced intracellular calcium levels, defective actin polymerization/depolymerization, and altered cytoskeletal rearrangement. In vivo, recruitment of eosinophils to the lungs of allergen-challenged Swap-70−/− mice, compared with wild-type mice, was significantly reduced, along with considerable attenuation of airway inflammation, indicated by diminished IL-5, IL-13, and TNF-α levels; reduced mucus secretion; and improved airway function. These findings suggest that regulation of eosinophil trafficking and migration by SWAP-70 is important for the development of eosinophilic inflammation after allergen exposure.
Dominant Th2 Differentiation of Human Regulatory T Cells upon Loss of FOXP3 Expression
Authors: Hansmann Leo , Schmidl Christian , Kett Janina , Steger Lena , Andreesen Reinhard , Hoffmann Petra , Rehli Michael , Edinger Matthias 
Published: December 2011

Abstract
CD4+CD25+FOXP3+ regulatory T cells (Treg) are pivotal for peripheral self-tolerance. They prevent immune responses to auto- and alloantigens and are thus under close scrutiny as cellular therapeutics for autoimmune diseases and the prevention or treatment of alloresponses after organ or stem cell transplantation. We previously showed that human Treg with a memory cell phenotype, but not those with a naive phenotype, rapidly downregulate expression of the lineage-defining transcription factor FOXP3 upon in vitro expansion. We now compared the transcriptomes of stable FOXP3+ Treg and converted FOXP3− ex-Treg by applying a newly developed intranuclear staining protocol that permits the isolation of intact mRNA from fixed, permeabilized, and FACS-purified cell populations. Whole-genome microarray analysis revealed strong and selective upregulation of Th2 signature genes, including GATA-3, IL-4, IL-5, and IL-13, upon downregulation of FOXP3. Th2 differentiation of converted FOXP3− ex-Treg occurred even under nonpolarizing conditions and could not be prevented by IL-4 signaling blockade. Thus, our studies identify Th2 differentiation as the default developmental program of human Treg after downregulation of FOXP3.
IL-2–Engineered nano-APC Effectively Activates Viral Antigen-Mediated T Cell Responses from Chronic Hepatitis B Virus-Infected Patients
Authors: Liu Mengya , Miao Tizong , Zhu Haoxiang , Symonds Alistair L. J. , Li Li , Schurich Anna , Maini Mala K. , Zhang Jiming , Kennedy Patrick T. F. , Li Suling , Wang Ping 
Published: December 2011

Abstract
Impaired function of virus-specific T cells resulting from virus persistence is one of the major mechanisms underlying the development of chronic hepatitis B viral infection. Previously, we found that IL-2 can restore the effector function of T cells rendered tolerant by Ag persistence. However, systemic administration of IL-2 induces organ pathology and expansion of T regulatory cells. In this study, we show that nano-APC with engineered HLA alleles and IL-2 deliver peptide–MHC complexes, costimulatory molecules, and IL-2 to Ag-responding T cells, resulting in enhanced expression of CD25 and activation of TCR signaling pathways, while suppressing PD-1 expression on viral-responding CD8 T cells from chronic hepatitis B virus patients. The enhanced activation of CD4 and CD8 T cells induced by IL-2–nano-APC was Ag dependent and IL-2–nano-APC did not affect T regulatory cells. At a size of 500 nm, the nano-APC effectively induce immune synapse formation on Ag-specific T cells and accumulate as free particles in the lymphoid organs. These attributes of IL-2–nano-APC or other bioadjuvant-engineered nano-APC have profound implications for their use as a therapeutic strategy in the treatment of chronic hepatitis B virus infection or other chronic viral diseases.