C. Hofstra

发表

Bronchoconstriction and airway hyperresponsiveness after ovalbumin inhalation in sensitized mice.

H. van Loveren, J. Garssen, H. Savelkoul, 1995, European journal of pharmacology.

Histamine H4 Receptor Mediates Chemotaxis and Calcium Mobilization of Mast Cells

P. Desai, R. Thurmond, W. Fung-Leung, 2003, Journal of Pharmacology and Experimental Therapeutics.

TSLP is differentially regulated by vitamin D3 and cytokines in human skin

R. de Waal Malefyt, S. Sadekova, K. Dechering, 2015, Immunity, inflammation and disease.

Suppression of the inflammatory response in experimental arthritis is mediated via estrogen receptor α but not estrogen receptor β

A. Boots, F. Dijcks, J. Dulos, 2010, Arthritis research & therapy.

CD97 in leukocyte trafficking.

P. Tak, H. van Eenennaam, A. Boots, 2010, Advances in experimental medicine and biology.

Prevention of Th2-like cell responses by coadministration of IL-12 and IL-18 is associated with inhibition of antigen-induced airway hyperresponsiveness, eosinophilia, and serum IgE levels.

M. Kool, I. van Ark, A. V. van Oosterhout, 1998, Journal of immunology.

Differential Effects of Endogenous and Exogenous Interferon- γ on Immunoglobulin E, Cellular Infiltration, and Airway Responsiveness in a Murine Model of Allergic Asthma

I. van Ark, A. V. van Oosterhout, F. Nijkamp, 1998 .

Antigen-stimulated lung CD4+ cells produce IL-5, while lymph node CD4+ cells produce Th2 cytokines concomitant with airway eosinophilia and hyperresponsiveness

M. Kool, I. van Ark, A. V. van Oosterhout, 1999, Inflammation Research.

CTLA4-IgG reverses asthma manifestations in a mild but not in a more "severe" ongoing murine model.

A. V. van Oosterhout, F. Nijkamp, B. V. van Esch, 2001, American journal of respiratory cell and molecular biology.

Allergen immunotherapy inhibits airway eosinophilia and hyperresponsiveness associated with decreased IL-4 production by lymphocytes in a murine model of allergic asthma.

I. van Ark, H. Savelkoul, M. Kapsenberg, 1998, American journal of respiratory cell and molecular biology.

Murine CTLA4-IgG treatment inhibits airway eosinophilia and hyperresponsiveness and attenuates IgE upregulation in a murine model of allergic asthma.

I. van Ark, B. Chan, A. V. van Oosterhout, 1997, American journal of respiratory cell and molecular biology.

Structure-based lead identification of ATP-competitive MK2 inhibitors.

J. Hornberg, C. Schultz-Fademrecht, B. Kazemier, 2011, Bioorganic & medicinal chemistry letters.

Cloning and pharmacological characterization of a fourth histamine receptor (H(4)) expressed in bone marrow.

Nicholas J. Carruthers, J. Pyati, T. Lovenberg, 2001, Molecular pharmacology.

A Potent and Selective Histamine H4 Receptor Antagonist with Anti-Inflammatory Properties

Lars Karlsson, James P. Edwards, P. Desai, 2004, Journal of Pharmacology and Experimental Therapeutics.

Tbt-1, a new T-box transcription factor induced in activated Th1 and CD8+ T cells

Xiao-Jun Ma, W. Fung-Leung, K. Ngo, 2000, Immunogenetics.

Org 214007-0: A Novel Non-Steroidal Selective Glucocorticoid Receptor Modulator with Full Anti-Inflammatory Properties and Improved Therapeutic Index

R. McGuire, W. Alkema, A. Grefhorst, 2012, PloS one.

A selective estrogen receptor alpha agonist (ORG 37663) suppresses inflammation and arthritis in mouse models

M. Lucassen, A. Boots, L. Joosten, 2006 .

p38 inhibition and not MK2 inhibition enhances the secretion of chemokines from TNF-α activated rheumatoid arthritis fibroblast-like synoviocytes.

J. Rullmann, H. van Eenennaam, M. V. van Vugt, 2013, Clinical and experimental rheumatology.

Vbeta8+ T lymphocytes are essential in the regulation of airway hyperresponsiveness and bronchoalveolar eosinophilia but not in allergen-specific IgE in a murine model of allergic asthma.

I. van Ark, H. Savelkoul, W. Cruikshank, 1998, Clinical and Experimental Allergy.

Histamine H4 Receptor Mediates Chemotaxis and Calcium Mobilization of Mast Cells

P. Desai, R. Thurmond, W. Fung-Leung, 2003, Journal of Pharmacology and Experimental Therapeutics.