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Peter Schmid-Grendelmeier

Publications and source records attributed to Peter Schmid-Grendelmeier.

27 records · Page 2Linked to original sources
PubMed2003

Human CD8 T cells of the peripheral blood contain a low CD8 expressing cytotoxic/effector subpopulation.

Heterogeneity of lymphocyte populations demonstrates the diversity of cellular immune responses and provide a better understanding of the immune system. CD3+ CD8+ T cells exhibit a low CD8 expressing (CD8low) population in flow cytometric analysis of peripheral blood T cells. In healthy donors, this population consists of 0.2-7.0% of all CD8 T cells. The majority of the CD8low T cell population showed an elevated expression of CD25, CD45RA, and CD95L, and low levels of CD28, CD62L and CD45RO. Circulating CD8low T cells resemble cytotoxic effector cells because they express cytolytic mediators and are able to execute cytotoxicity. A restricted T cell receptor profile with increased Vbeta9, Vbeta14 and Vbeta23 expression was observed and the CD8low T cell population contain Epstein-Barr virus-specific T cells. Therefore, the CD8low population represent a subset of activated CD8 effector T cells, resulting most probably from a continuous and/or balanced immune response to intracellular pathogens.

CD8 Antigens↗
PubMed2003

Native Art v 1 and recombinant Art v 1 are able to induce humoral and T cell-mediated in vitro and in vivo responses in mugwort allergy.

BACKGROUND: Mugwort pollen is an important allergen source in hay fever and pollen-related food allergy. Little is known about the clinical relevance of the major mugwort allergen Art v 1 and its importance in allergy. OBJECTIVE: In this study we aimed to investigate the allergenicity of mugwort extract compared with the allergenicity of native (n)Art v 1 and recombinant (r)Art v 1, one major allergen of mugwort, in vivo and in vitro. METHODS: Thirty-two patients allergic to mugwort and 10 control subjects were investigated by means of skin prick and nasal provocation testing with different concentrations of mugwort extract, nArt v 1, and rArt v 1. nArt v 1 was purified from aqueous mugwort extract, and rArt v 1 was cloned, expressed in Escherichia coli, and then purified. The in vitro allergenicity was measured by means of ImmunoCAP, ELISA, ELISA-inhibition experiments, and T-cell proliferation assays. RESULTS: nArt v 1 and rArt v 1 were able to elicit positive in vivo and in vitro reactions. The IgE-binding capacity, as determined by means of ELISA, was slightly higher for nArt v 1 than for rArt v 1, and both allergens were able to induce T-cell proliferation in sensitized patients. However, rArt v 1 elicited a reduced response in skin and nasal provocation tests compared with nArt v 1. Compared with mugwort extract, both nArt v 1 and rArt v 1 showed lower sensitivity in patients with mugwort allergy in vivo. CONCLUSIONS: Art v 1, either in its native or recombinant form, is able to induce allergic reactions in patients with mugwort allergy. rArt v 1 induced comparable humoral and cell-mediated responses in vitro but showed reduced in vivo allergenicity compared with biochemically purified nArt v 1.

Adult↗
PubMed2002

Eosinophils express functional IL-13 in eosinophilic inflammatory diseases.

IL-13 is an immunoregulatory and effector cytokine in allergic diseases such as bronchial asthma. A variety of immune and non-immune cells are known as IL-13 producers. In this study we investigated whether and under what conditions human eosinophils generate IL-13. Freshly isolated highly purified peripheral blood eosinophils from patients with several eosinophilic inflammatory diseases and from normal control individuals were investigated. We observed that blood eosinophils from patients suffering from bronchial asthma, atopic dermatitis, parasitic infections, hypereosinophilic syndrome, and idiopathic eosinophilic esophagitis expressed IL-13, as assessed by ELISA, ELISPOT assay, flow cytometry, and immunocytochemistry. By using nasal polyp tissues and immunohistochemistry, we demonstrated IL-13 expression in eosinophils under in vivo conditions. In contrast, blood eosinophils from control individuals as well as blood neutrophils from both eosinophilic and control patients did not produce detectable IL-13 levels. However, when blood eosinophils from control individuals were stimulated with GM-CSF or IL-5 in vitro, they generated IL-13 mRNA and protein, suggesting that IL-13 expression by eosinophils under inflammatory conditions is a cytokine-driven process. Stimulation of blood eosinophils containing IL-13 by eotaxin resulted in a rapid release of this cytokine. Eosinophil-derived IL-13 was functional, as it increased the surface expression of the low affinity IgE receptor (CD23) on purified B cells. In conclusion, human eosinophils are able to produce and release functional IL-13 in eosinophilic inflammatory responses.

Adult↗
PubMed2002

T cells and eosinophils cooperate in the induction of bronchial epithelial cell apoptosis in asthma.

BACKGROUND: Asthma is an inflammatory airway disease associated with an infiltration of T cells and eosinophils, increased levels of pro-inflammatory cytokines, and shedding of bronchial epithelial cells (ECs). OBJECTIVE: Shedding of bronchial ECs is characterized by loss of the normal bronchial pseudostratified epithelium and the maintenance of a few basal cells on a thickened basement membrane. The aim of this study was to investigate whether, and by which mechanism, T cells and eosinophils can cause damage to airway ECs. METHODS: Bronchial ECs, cultured and exposed to cytokines, eosinophil cationic protein, activated T cells, and eosinophils were studied for the expression of apoptosis receptors (flow cytometry, immunoblotting, and RNA expression) and for the susceptibility for undergoing apoptosis. In addition, bronchial biopsy specimens from patients with asthma were evaluated for EC apoptosis. RESULTS: We demonstrate herein that the respiratory epithelium is an essential target of the inflammatory attack by T cells and eosinophils. Bronchial ECs underwent cytokine-induced cell death with DNA fragmentation and morphologic characteristics of apoptosis mediated by activated T cells and eosinophils. T cell- and eosinophil-induced EC apoptosis was blocked by inhibition of IFN-alpha and TNF-alpha; the Fas ligand-Fas pathway appears to be less important. Recombinant eosinophil cationic protein induced mainly necrosis of ECs. Furthermore, we demonstrated in situ apoptotic features of ECs in bronchial biopsy specimens of asthmatic patients. CONCLUSION: T cell- and eosinophil-induced apoptosis represents a key pathogenic event leading to EC shedding in asthma.

Apoptosis↗
PubMed2002

High serum thymus and activation-regulated chemokine levels in the lymphocytic variant of the hypereosinophilic syndrome.

The idiopathic hypereosinophilic syndrome is associated with expansion of an IL-5-producing T-cell subset in a subgroup of patients. Identification of such patients is critical to adequate management because there is some evidence that they present an increased risk for development of T-cell lymphoma. Although the T(H)2-like cells often bear an aberrant surface phenotype and can readily be detected with flow cytometry, we now show that lymphocyte phenotyping might be normal in some cases. In contrast, serum thymus and activation-regulated chemokine levels are consistently increased in such patients compared with others with persistent idiopathic hyper-eosinophilia and could therefore represent a useful diagnostic tool.

Adolescent↗
PubMedDate not supplied

Panniculitis after subcutaneous injection of interferon beta in a multiple sclerosis patient.

BACKGROUND: Interferons are used in the immune therapy of multiple sclerosis, Kaposi's sarcoma, hepatitis and melanoma based on their antiviral, immunoregulatory and antitumor activities. We report a rare side effect observed during treatment of multiple sclerosis with subcutaneous interferon beta injections. OBSERVATIONS: A 44-year-old patient diagnosed with multiple sclerosis received immune therapy with 6 Mio IU recombinant interferon-beta (IFN-beta) every other day. After 4 years of subcutaneous interferon injections painful indurations appeared directly at and adjacent to the injection sites on the thighs, arms and abdomen. Pain in the thighs made walking almost impossible and required therapy with opiates. After changing to another interferon-beta medication the symptoms improved. Subsequent treatment with doxycycline for 3 weeks was of no additional benefit. CONCLUSIONS: Panniculitis at the injection sites is a rare event but has a significant impact on the quality of life during interferon therapy.

Adjuvants, Immunologic↗