ISSN:0105-4538    

DOI:10.1111/j.1398-9995.1995.tb02476.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

ISSN:0105-4538    

DOI:10.1111/j.1398-9995.1995.tb04276.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

ISSN:0105-4538    

DOI:10.1111/j.1398-9995.1995.tb04279.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

ISSN:0105-4538    

DOI:10.1111/j.1398-9995.1995.tb04280.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

ISSN:0105-4538    

DOI:10.1111/j.1398-9995.1995.tb04278.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

ISSN:0105-4538    

DOI:10.1111/j.1398-9995.1995.tb04281.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

ISSN:0105-4538    

DOI:10.1111/j.1398-9995.1995.tb04340.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

The link between immunoglobulin E (IgE) antibodies and environmental allergens, allergic sensitization and atopic diseases such as asthma, rhinitis and eczema is well established, yet treatment of these diseases is largely symptomatic and fails to correct the underlying immune disorder. B‐cell production of IgE depends on interleukin 4 (IL‐4) and is inhibited by interferon (IFN‐γ). These cytokines are produced by T‐helper 2 (Th2) and T‐helper 1 (Th1) CD4+T cells respectively. In atopic dermatitis skin and asthmatic lung, Th2 cells predominate but antigen‐specific CD4+T‐cell clones derived from peripheral blood are a mixture of Th1, Th2, and Th0. Circulating allergen‐specific CD4+T cells differentiate into Th1‐ and Th2‐like clones in the presence of IL‐12 and IL‐4 respectively. In rats, CD8+T cells are potent regulators of IgE responsesin vivo, although the mechanism for this is still unclear. CD8+T‐cell depletion in immunized animals prolonged the IgE response but prior depletion did not. Indeed, prior depletion of CD8+T cells actually inhibited IgE production, suggesting that there may be more than one type of IgE regulatory CD8+T cell. This was supported by the observation that CD8+T cells inhibited the differentiation of both Th1 and Th2 CD4+T cellsin vitroas well as IL‐4‐but not IL‐2‐induced Th2 CD4+T‐cell growth. The existence of distinct CD8+T‐cell subsets is supported by the observation that IL‐4 and IFN‐γ regulate the growth and differentiation of CD8+T cells. IL‐4 inhibits the development of CD8+T cells that produce IL‐2 and IL‐6 and enhances the generation of cells that make IL‐4 and IL‐5. A combination of IL‐4 and anti‐IFN‐γ enhanced IFN‐γ and IL‐10 production. Studies are continuing to characterize different CD8+T‐cell subs

ISSN:0105-4538    

DOI:10.1111/j.1398-9995.1995.tb04268.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

SummaryImmuno‐histopathological studies of conjunctival tissue biopsied from patients with non‐sight‐threatening allergic conjunctivitis or with sight‐threatening allergic keratoconjunctivitis should lead to more effective management of these eye conditions, based on the specific cellular involvement. The major difference between these two categories of eye disease was the occurrence of T‐lymphocytes, which were absent in the former but prominent in the sight‐threatening disorders. Seasonal and perennial allergic conjunctivitis both showed a heavy mast cell increase, due to infiltration of mucosal type mast cells, and allergen challenge studies linked mast cell histamine release to the early phase reaction occurring within 20 minutes. A second histamine peak at six hours after challenge might implicate basophils (or refractory mast cells) and was accompanied by a rise in eosinophil cationic protein. In sight‐threatening, chronic allergic keratoconjunctivitis the responses were clearly directed by T‐cells, themselves the primary effector cell in atopic keratoconjunctivitis, whereas vernal keratoconjunctivitis displayed a T‐cell driven eosinophilia, with increased expression of the adhesion molecules involved in tissue invasion by these cells. Appropriate therapies for each different category of conjunctivitis should be based on the specific immunopathology, and directed at the activated cell types that are primarily responsible for th

ISSN:0105-4538    

DOI:10.1111/j.1398-9995.1995.tb04251.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Fluticasone propionate is a new corticosteroid based on the androstane nucleus. It is more lipophilic than beclomethasone dipropionate (BDP) and budesonide, and binds more avidly to human lung tissue. It has an absolute affinity (KD) of 0.5 nM for the glucocorticoid receptor and a relative receptor aflinity 1.5‐ and 3.0‐times greater than that of beclomethasone‐17‐monopropionate (17‐BMP) and budesonide, respectively. The rate of association with the receptor is faster and the rate of dissociation slower than with standard corticosteroids. As a result, the half‐life of the corticosteroid‐receptor complex is>10 h. Fluticasone propionate is also highly selective for the glucocorticoid receptor, with little or no activity at other steroid receptors. Pretreatment with fluticasone propionate signiflcantly inhibits the increase in mast cell numbers in the nasal mucosa of rats chronically exposed to toluene di‐isocyanate (TDI), and suppresses TDI‐induced mast cell degranulation. It is more potentin vitrothan dexamethasone, BDP and budesonide in inhibiting anti‐CD3‐induced human T‐lymphocyte proliferation, in attenuating tumour necrosis factor‐α‐induced endothelial cell adhesion molecule expression, and in increasing secretory leucocyte protease inhibitor levels in airway epithelial cells. It is also more potent and longer‐acting than other corticosteroids in inhibiting oedema formation, interleukin‐5 (IL‐5)‐induced blood eosinophilia, and IL‐5‐ or platelet activating factor‐stimulated eosinophil accumulation in the lung. Fluticasone propionate therefore has increased intrinsic glucocorticoid potency a

ISSN:0105-4538    

DOI:10.1111/j.1398-9995.1995.tb02735.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY