Anti-allergic drug olopatadine suppresses murine contact hypersensitivity and downmodulates antigen-presenting ability of epidermal Langerhans cells.

[1]  H. Tokumitsu,et al.  Interaction of S100 proteins with the antiallergic drugs, olopatadine, amlexanox, and cromolyn: identification of putative drug binding sites on S100A1 protein. , 2002, Biochemical and biophysical research communications.

[2]  Y. Tokura,et al.  Dominant expression of CXCR3 is associated with induced expression of IP-10 at hapten-challenged sites of murine contact hypersensitivity: a possible role for interferon-gamma-producing CD8(+) T cells in IP-10 expression. , 2002, Journal of dermatological science.

[3]  J. Conner,et al.  Nerve growth factor, neuropeptides, and mast cells in ultraviolet-B-induced systemic suppression of contact hypersensitivity responses in mice. , 2002, The Journal of investigative dermatology.

[4]  F. Graziano,et al.  Olopatadine inhibits anti-immunoglobulin E-stimulated conjunctival mast cell upregulation of ICAM-1 expression on conjunctival epithelial cells. , 2001, Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology.

[5]  A. Ishii,et al.  Effects of olopatadine hydrochloride on the cutaneous vascular hyperpermeability and the scratching behavior induced by poly-L-arginine in rats. , 2001, Japanese journal of pharmacology.

[6]  D. Sauder,et al.  Insights into molecular mechanisms of contact hypersensitivity gained from gene knockout studies , 2001, Journal of leukocyte biology.

[7]  R. Donato,et al.  S100: a multigenic family of calcium-modulated proteins of the EF-hand type with intracellular and extracellular functional roles. , 2001, The international journal of biochemistry & cell biology.

[8]  D. Spangler,et al.  A comparison of the relative efficacy and clinical performance of olopatadine hydrochloride 0.1% ophthalmic solution and ketotifen fumarate 0.025% ophthalmic solution in the conjunctival antigen challenge model. , 2000, Clinical therapeutics.

[9]  F. Graziano,et al.  Olopatadine inhibits TNFα release from human conjunctival mast cells , 2000 .

[10]  S. Xu,et al.  Inhibition of histamine-induced human conjunctival epithelial cell responses by ocular allergy drugs. , 1999, Archives of ophthalmology.

[11]  H. Maeta,et al.  Three distinct anti-allergic drugs, amlexanox, cromolyn and tranilast, bind to S100A12 and S100A13 of the S100 protein family. , 1999, The Biochemical journal.

[12]  D. Wakefield,et al.  Mast cell activation and migration to lymph nodes during induction of an immune response in mice. , 1998, The Journal of clinical investigation.

[13]  H. Kase,et al.  Unique binding pocket for KW-4679 in the histamine H1 receptor. , 1998, European journal of pharmacology.

[14]  H. Ishii,et al.  Effects of KW-4679, a new orally active antiallergic drug, on antigen-induced bronchial hyperresponsiveness, airway inflammation and immediate and late asthmatic responses in guinea pigs. , 1996, International archives of allergy and immunology.

[15]  I. Miki,et al.  KW-4679, an antiallergic drug, inhibits the production of inflammatory lipids in human polymorphonuclear leukocytes and guinea pig eosinophils. , 1996, International archives of allergy and immunology.

[16]  K. Ohmori,et al.  KW‐4679‐induced inhibition of tachykininergic contraction in the guinea‐pig bronchi by prejunctional inhibition of peripheral sensory nerves , 1996, British journal of pharmacology.

[17]  A. Enk,et al.  Contact sensitivity as a model for T-cell activation in skin. , 1995, Journal of Investigative Dermatology.

[18]  F. Furukawa,et al.  ACCESSORY CELL ABILITY OF LANGERHANS CELLS FOR SUPERANTIGEN IS RESISTANT TO ULTRAVIOLET‐B LIGHT , 1994, Photochemistry and photobiology.

[19]  C. Chang,et al.  Immunosuppressive effects of azelastine hydrochloride on contact hypersensitivity and T-cell proliferative response: a comparative study with FK-506. , 1994, The Journal of investigative dermatology.

[20]  Y. Tokura,et al.  Superantigenic staphylococcal exotoxins induce T-cell proliferation in the presence of Langerhans cells or class II-bearing keratinocytes and stimulate keratinocytes to produce T-cell-activating cytokines. , 1994, The Journal of investigative dermatology.

[21]  T. Kupper,et al.  The activated keratinocyte: a model for inducible cytokine production by non-bone marrow-derived cells in cutaneous inflammatory and immune responses. , 1990, The Journal of investigative dermatology.

[22]  J. Hornung,et al.  Normal keratinization in a spontaneously immortalized aneuploid human keratinocyte cell line , 1988, The Journal of cell biology.

[23]  G. Mierau,et al.  S-100 protein immunohistochemistry and electron microscopy in the diagnosis of Langerhans cell proliferative disorders: a comparative assessment. , 1986, Ultrastructural pathology.

[24]  J. Streilein,et al.  Langerhans cells: antigen presenting cells of the epidermis. , 1984, Immunobiology.

[25]  T. Nakajima,et al.  An immunoperoxidase study of S-100 protein distribution in normal and neoplastic tissues , 1982, The American journal of surgical pathology.

[26]  R. Wollmann,et al.  Distribution of S-100 protein outside the central nervous system , 1982, Brain Research.