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  • Articles: DFG German National Licenses  (8)
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  • Articles: DFG German National Licenses  (8)
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  • 1
    Electronic Resource
    Electronic Resource
    Immunologic and non-immunologic release of histamine and tryptase from human heart mast cells (1995)
    Springer
    Inflammation research 44 (1995), S. S22 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01674377
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Histamine release from human basophils by pepstatin A (1985)
    Springer
    Inflammation research 16 (1985), S. 306-309 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Pepstatin A, a pentapeptide isolated from cultures of actinomycetes, induced histamine secretion from human basophils in the concentration range of 3×10−7 to 10−4 M. The characteristics of this reaction were similar to those of f-met-peptide-induced histamine release: pepstatin A-induced release required Ca2+ and the release reaction was complete within 2 min at 22 or 37°C, but did not occur at 4°C. Release by both pepstatin a and f-met-peptide was reversibly inhibited by two non-releasing analogs of f-met-peptide, CBZ-Phe-Met and BOC-Met-Leu-Phe, Further, there was complete cross-desensitization between pepstatin A and f-met-peptide, while cells desensitized to pepstatin A released normally with anti-IgE and vice versa. A variety of pharmacological agents had similar effects on both pepstatin A and f-met-peptide-induced release (e.g., no enhancement with D2O; marked enhancement with cytochalasin B). We suggest that pepstatin A induces histamine release from human basophils by activating a cell surface receptor(s), also activated by the synthetic tripeptide f-met-peptide.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01982863
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Role of human FcεRI+ cells in HIV-1 infection (2001)
    Copenhagen : Munksgaard International Publishers
    Immunological reviews 179 (2001), S. 0 
    Details
    ISSN: 1600-065X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary: Enhanced serum IgE levels in adults and children with HIV-1 infection could be a marker of poor prognosis. HIV-1 infection is believed to involve a switch toward a “TH2-like” cytokine pattern. HIV-1 gp120 from different clades is a potent stimulus for histamine release from human basophils and mast cells. Gp120 also induces IL-4 and IL-13 synthesis from basophils. It functions as a viral superantigen by interacting with the VH3 region of IgE to induce mediator release from human FcεRI+ cells. The chemokine receptor CCR3, which binds the chemokines eotaxin and RANTES, is expressed by basophils and lung mast cells. By interacting with the CCR3 receptor on FcεRI+ cells, HIV-1 Tat protein is a potent chemoattractant for basophils and lung mast cells. Tat protein also induces IL-4 and IL-13 release from basophils. Incubation of basophils with Tat protein upregulates the surface expression of the CCR3 receptor, a co-receptor of HIV-1 infection. Extracellular Tat affects the directional migration of human FcεRI+ cells, CCR3 expression and TH2 cytokines release. We have shown that HIV-1 proteins gp120 and Tat trigger the release of cytokines critical for TH2 polarization from FcεRI+ cells through two distinct mechanisms. In addition, Tat upregulates the β-chemokine receptor CCR3, making FcεRI+ cells more susceptible to infection with CCR3 tropic HIV-1 isolates.This paper is dedicated to Rita Levi-Montalcini who first suggested an involvement of FcεRI+ cells in HIV-1 infection. This work was supported by a grant from the Istituto Superiore Sanità (AIDS project 40B.64 and 40A.67), CNR (Target project Biotechnology No. 99.00216.PF31 and No. 99.00401. PF49) and MURST (Rome, Italy).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1600-065X.2001.790113.x
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  • 4
    Electronic Resource
    Electronic Resource
    IgE-Mediated Basophil Phenomena: Quantitation, Control, Inflammatory Interactions (1978)
    Oxford, UK : Blackwell Publishing Ltd
    Immunological reviews 41 (1978), S. 0 
    Details
    ISSN: 1600-065X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-065X.1978.tb01464.x
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  • 5
    Electronic Resource
    Electronic Resource
    Italian immunology well but hoping to do better (2001)
    [s.l.] : Nature Publishing Group
    Nature 413 (2001), S. 771-771 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Sir I was delighted to read, in the same issue, your News Feature on science in Italy (Nature 412, 264–265; 2001) and your Naturejobs article on careers in clinical immunology (Naturejobs 19 July, 5; 2001). However, ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/35101764
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    Paper (German National Licenses)
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  • 6
    Electronic Resource
    Electronic Resource
    Milestones in the biology and pharmacology of histamine H1-receptor antagonists (1997)
    Oxford, UK : Blackwell Publishing Ltd
    Allergy 52 (1997), S. 0 
    Details
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Daniele Bovet's pioneering discovery that a series of compounds possessing anti-histamine activity reduced the symptoms of anaphylaxis provided the proof that histamine plays a pivotal role as a mediator of allergic reactions. Basophils and mast cells are the major sources of histamine in man and they are thus one of the primary effector cells of allergic inflammation. Some H1-receptor antagonists posseses a variety of antiinflammatory activity to H1-- antagonism in vitro and in vivo. This promising area should be explored further and much remains to be done in the evaluation of the immunodulatory effects of anti-histamines.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1398-9995.1997.tb04806.x
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  • 7
    Electronic Resource
    Electronic Resource
    Cardiovascular and Metabolic Effects of Peptide Leukotrienes in Man (1988)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 524 (1988), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1988.tb38555.x
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  • 8
    Electronic Resource
    Electronic Resource
    Immunological Modulation of Human Cardiac Mast Cells (1999)
    Springer
    Neurochemical research 24 (1999), S. 1195-1202 
    Details
    ISSN: 1573-6903
    Keywords: Anaphylaxis ; atherosclerosis ; heart ; histamine ; leukotrienes ; mast cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Human mast cells, by elaborating various cytokines, chemokines and proinflammatory mediators play a complex role in several allergic and inflammatory disorders. Mast cells have been identified in human heart tissue in close proximity to the sarcolemma, in perivascular and adventitial locations and in the shoulder region of coronary atheroma. Human heart mast cells (HHMC) can be isolated from patients undergoing heart transplantation and can be immunologically activated in vitro to induce the release of tryptase, chymase, cysteinyl leukotriene C4 and prostaglandin D2. Several cytokines (e.g., stem cell factor and TNF-α) reside in secretory granules of HHMC. Mast cell density is increased in the hearts of patients with ischemic and idiopathic dilated cardiomyopathy. Cardiac mast cells might contribute to the evolution of atherosclerosis, dilated cardiomyopathy, cardiac and systemic anaphylaxis through the release of cytokines and vasoactive and proinflammatory mediators.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1020776807187
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    Paper (German National Licenses)
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