نتایج جستجو برای: lymphotoxin a gene

تعداد نتایج: 13657811  

Journal: :Journal of medical genetics 1999
E Trabetti C Patuzzo G Malerba R Galavotti L C Martinati A L Boner P F Pignatti

Tumour necrosis factor (TNF) is a proinflammatory cytokine that increases human airway tissue responsiveness and is considered a candidate gene for asthma. Two common polymorphisms (LTalphaNcoI and TNFalpha-308) in the TNF gene complex were studied in 600 subjects from 131 Italian families with atopic asthmatic children. Skin prick test (SPT), total IgE levels, atopy (defined as increased IgE l...

Journal: :Genetics and molecular research : GMR 2014
Y Y Zhang S Y Wang Y W Miao W Z Li Q L Zhang F Q Li L X Liu H L Huo J L Huo

The lymphotoxin beta receptor (LTβR) is a member of the tumor necrosis factor family of receptors (TNFR). It plays a role in regulating lymphoid organogenesis and homeostasis of the immune system. In the present study, the full coding region of a putative LTβR gene of Sus scrofa was amplified by reverse transcription-polymerase chain reaction (RT-PCR) and cloned for the first time (accession No...

2014
Jadwiga Bienkowska Norm Allaire Alice Thai Jaya Goyal Tatiana Plavina Ajay Nirula Megan Weaver Charlotte Newman Michelle Petri Evan Beckman Jeffrey L. Browning

A subset of patients with autoimmune diseases including rheumatoid arthritis (RA) and lupus appear to be exposed continually to interferon (IFN) as evidenced by elevated expression of IFN induced genes in blood cells. In lupus, detection of endogenous chromatin complexes by the innate sensing machinery is the suspected driver for the IFN, but the actual mechanisms remain unknown in all of these...

Journal: :Cancer discovery 2014
Kristina Heinig Marcel Gätjen Michael Grau Vanessa Stache Ioannis Anagnostopoulos Kerstin Gerlach Raluca A Niesner Zoltan Cseresnyes Anja E Hauser Peter Lenz Thomas Hehlgans Robert Brink Jörg Westermann Bernd Dörken Martin Lipp Georg Lenz Armin Rehm Uta E Höpken

UNLABELLED In human chronic lymphocytic leukemia (CLL) pathogenesis, B-cell antigen receptor signaling seems important for leukemia B-cell ontogeny, whereas the microenvironment influences B-cell activation, tumor cell lodging, and provision of antigenic stimuli. Using the murine Eμ-Tcl1 CLL model, we demonstrate that CXCR5-controlled access to follicular dendritic cells confers proliferative s...

Journal: :The Journal of biological chemistry 2006
Claudia Bossen Karine Ingold Aubry Tardivel Jean-Luc Bodmer Olivier Gaide Sylvie Hertig Christine Ambrose Jürg Tschopp Pascal Schneider

Ligands of the tumor necrosis factor superfamily (TNFSF) (4-1BBL, APRIL, BAFF, CD27L, CD30L, CD40L, EDA1, EDA2, FasL, GITRL, LIGHT, lymphotoxin alpha, lymphotoxin alphabeta, OX40L, RANKL, TL1A, TNF, TWEAK, and TRAIL) bind members of the TNF receptor superfamily (TNFRSF). A comprehensive survey of ligand-receptor interactions was performed using a flow cytometry-based assay. All ligands engaged ...

Journal: :Proceedings of the National Academy of Sciences 1973

Journal: :Infection and immunity 2012
Arielle Glatman Zaretsky Jonathan S Silver Marie Siwicki Amy Durham Carl F Ware Christopher A Hunter

B cell responses are required for resistance to Toxoplasma gondii; however, the events that lead to production of class-switched antibodies during T. gondii infection have not been defined. Indeed, mice challenged with the parasite exhibited an expansion of T follicular helper cells and germinal center B cells in the spleen. Unexpectedly, this was not associated with germinal center formation a...

Journal: :The Journal of Experimental Medicine 2001
Paul D. Rennert Paula S. Hochman Richard A. Flavell David D. Chaplin Sundararajan Jayaraman Jeffrey L. Browning Yang-Xin Fu

Lymph nodes (LNs) are important sentinal organs, populated by circulating lymphocytes and antigen-bearing cells exiting the tissue beds. Although cellular and humoral immune responses are induced in LNs by antigenic challenge, it is not known if LNs are essential for acquired immunity. We examined immune responses in mice that lack LNs due to genetic deletion of lymphotoxin ligands or in utero ...

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