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160 results found
WELLS AU, LORIMER S, MAJUMDAR S, et al., 1995, FIBROSING ALVEOLITIS IN SYSTEMIC-SCLEROSIS - INCREASE IN MEMORY T-CELLS IN LUNG INTERSTITIUM, EUROPEAN RESPIRATORY JOURNAL, Vol: 8, Pages: 266-271, ISSN: 0903-1936
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- Citations: 52
Caplen NJ, Alton EWFW, Middleton PG, et al., 1995, Erratum: Liposome-mediated CFTR gene transfer to the nasal epithelium of patients with cystic fibrosis (Nature Medicine (January 1995) 1 (39-46)), Nature Medicine, Vol: 1, ISSN: 1078-8956
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- Citations: 1
CAPLEN NJ, ALTON E, MIDDLETON PG, et al., 1995, LIPOSOME-MEDIATED CFTR GENE-TRANSFER TO THE NASAL EPITHELIUM OF PATIENTS WITH CYSTIC-FIBROSIS, NATURE MEDICINE, Vol: 1, Pages: 39-46, ISSN: 1078-8956
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- Citations: 653
DEVALIA JL, GODFREY RWA, SAPSFORD RJ, et al., 1994, NO EFFECT OF HISTAMINE ON HUMAN BRONCHIAL EPITHELIAL-CELL PERMEABILITY AND TIGHT JUNCTIONAL INTEGRITY IN-VITRO, EUROPEAN RESPIRATORY JOURNAL, Vol: 7, Pages: 1958-1965, ISSN: 0903-1936
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- Citations: 20
JEFFERY PK, 1994, COMPARATIVE MORPHOLOGY OF THE AIRWAYS IN ASTHMA AND CHRONIC OBSTRUCTIVE PULMONARY-DISEASE, Workshop on Asthma and Bronchial Inflammation, Publisher: AMER LUNG ASSOC, Pages: S6-S13, ISSN: 1073-449X
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- Citations: 76
Shahzeidi S, Jeffery PK, Laurent GJ, et al., 1994, Increased type I procollagen mRNA transcripts in the lungs of mice during the development of bleomycin-induced fibrosis., Eur Respir J, Vol: 7, Pages: 1938-1943, ISSN: 0903-1936
In this study, in situ hybridization has been used to investigate the localization of type I procollagen messenger ribonucleic acid (mRNA) in normal lung, and in the lungs of mice during the development of bleomycin-induced pulmonary fibrosis. Lung fibrosis was induced by a single intratracheal instillation of bleomycin sulphate (6 mg.kg-1 body weight), and tissues examined at times up to 35 days thereafter. Tissue transcripts of alpha 2(I) procollagen mRNA were visualized after hybridization with 35S-labelled riboprobes. Hybridization signals were associated with alveolar interstitial cells throughout the normal lung, with additional areas of dense hybridization signals observed subpleurally. Three days following administration of bleomycin, there was no apparent change in the pattern of hybridization. By 10 days, foci of intense hybridization signals indicative of gene activation were observed associated with individual cells in the alveolar interstitium. At 21 days, the increase in hybridization signals appeared to be associated with greater numbers of cells rather than highly activated cells. These results demonstrate that procollagen genes are normally expressed in the mouse lung, and that during bleomycin-induced pulmonary fibrosis hybridization signals increase, suggesting that both enhanced gene expression by individual cells and increased numbers of cells expressing the type I procollagen gene are involved in the pathogenetic mechanism.
Jeffery PK, 1994, Comparative morphology of the airways in asthma and chronic obstructive pulmonary disease., Am J Respir Crit Care Med, Vol: 150, Pages: S6-13, ISSN: 1073-449X
Asthma and chronic obstructive pulmonary disease (COPD) are complex conditions with imprecise definitions that make definitive morphological comparisons difficult. Asthma may be divided into extrinsic (allergic), intrinsic (late onset), and occupational forms. The airways in fatal asthma are occluded by markedly tenacious plugs of exudate and mucus; there is fragility of airway surface epithelium, thickening of the reticular basement membrane, and bronchial vessel dilatation, congestion, and edema. There is enlargement of bronchial smooth muscle and also of submucosal gland mass, particularly in medium-sized bronchi. There is increased inflammatory infiltrate comprising activated lymphocytes and eosinophils with release of granular content in the latter; the allergic inflammation is associated with gene expression for interleukins IL-4 and IL-5 (ie, TH2 phenotype) and also GMCSF and TNF alpha. Many of these changes are already present in mild forms of asthma. In comparison, three conditions contribute to COPD: (1) In chronic bronchitis there is inflammation associated with mucous hypersecretion, enlargement of tracheo-bronchial submucosal glands, and a disproportionate increase of acidic mucus. The reticular basement membrane is not consistently thickened. (2) In small (peripheral) airways disease there is a macrophage bronchiolitis, mucous metaplasia and hyperplasia, increased intraluminal mucus, increased wall muscle, fibrosis, and airway stenoses. Respiratory bronchiolitis and loss of alveolar wall attachments are important lesions. (3) Emphysema involves elastolytic destruction of the alveolar wall; its overall severity, rather than type, appears to be an important determinant of chronic irreversible deterioration of airflow in COPD.
GODFREY RWA, SEVERS NJ, JEFFERY PK, 1994, A COMPARISON BETWEEN THE EPITHELIAL TIGHT JUNCTION MORPHOLOGY OF HUMAN EXTRAPULMONARY BRONCHI AND RAT TRACHEA, EUROPEAN RESPIRATORY JOURNAL, Vol: 7, Pages: 1409-1415, ISSN: 0903-1936
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- Citations: 7
JEFFERY PK, 1994, STRUCTURAL-CHANGES IN ASTHMA, Scientific Program on Airways and Vascular Remodelling in Asthma and Cardiovascular Disease - Implications for Therapeutic Intervention, Publisher: ACADEMIC PRESS LTD-ELSEVIER SCIENCE LTD, Pages: 3-19
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- Citations: 9
ALTON E, MIDDLETON PG, CAPLEN NJ, et al., 1993, NONINVASIVE LIPOSOME-MEDIATED GENE DELIVERY CAN CORRECT THE ION-TRANSPORT DEFECT IN CYSTIC-FIBROSIS MUTANT MICE, NATURE GENETICS, Vol: 5, Pages: 135-142, ISSN: 1061-4036
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- Citations: 389
GODFREY RWA, SEVERS NJ, JEFFERY PK, 1993, STRUCTURAL ALTERATIONS OF AIRWAY EPITHELIAL TIGHT JUNCTIONS IN CYSTIC-FIBROSIS - COMPARISON OF TRANSPLANT AND POSTMORTEM TISSUE, AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, Vol: 9, Pages: 148-156, ISSN: 1044-1549
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- Citations: 23
SHAHZEIDI S, MULIER B, DECROMBRUGGHE B, et al., 1993, ENHANCED TYPE-III COLLAGEN GENE-EXPRESSION DURING BLEOMYCIN-INDUCED LUNG FIBROSIS, THORAX, Vol: 48, Pages: 622-628, ISSN: 0040-6376
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- Citations: 35
Shahzeidi S, Mulier B, de Crombrugghe B, et al., 1993, Enhanced type III collagen gene expression during bleomycin induced lung fibrosis., Thorax, Vol: 48, Pages: 622-628, ISSN: 0040-6376
BACKGROUND: Intratracheal instillation of bleomycin into mice leads to deposition of collagen in the lung and fibrosis, but the mechanism for this is poorly understood. Enhanced collagen gene expression, increased collagen synthesis, decreased collagen degradation, and proliferation of fibroblasts have all been proposed as possible contributors. To obtain information on the activity of collagen producing cells at an early stage in the development of pulmonary fibrosis in situ hybridisation was used to detect and localise products of the type III procollagen gene. In addition, assay of type III procollagen gene expression was performed using dot-blot analysis of lung RNA extracts. METHODS: Lung fibrosis was induced in mice by intratracheal instillation of bleomycin sulphate (6 mg/kg body weight) and tissues were examined after three, 10, 21 and 35 days. RNA-RNA hybridisation was accomplished with riboprobes labelled with sulphur-35 which were generated from a 1.7 kb mouse procollagen a1(III) cDNA. In situ hybridisation was performed on sections fixed in paraformaldehyde and embedded in paraffin wax and steady state values of type III procollagen mRNA were assayed by dot-blot analysis of total lung RNA extracted by guanidium isothiocyanate. RESULTS: Data obtained using both techniques suggest that type III procollagen gene expression was enhanced in bleomycin induced fibrosis and that expression was maximal between 10 and 35 days after a single dose of bleomycin. The most active cells were located in interstitial areas around the conducting airways, although these cells were usually seen in areas with no histological evidence of fibrosis. Regions with the most advanced fibrosis, as assessed by histological methods, rarely contained cells with activity above the threshold detectable by this technique. CONCLUSIONS: These results suggest that activation of interstitial fibroblasts, with enhanced type III collagen gene expression, forms at least part of the mechanism lead
ROGERS AV, DEWAR A, CORRIN B, et al., 1993, IDENTIFICATION OF SEROUS-LIKE CELLS IN THE SURFACE EPITHELIUM OF HUMAN BRONCHIOLES, EUROPEAN RESPIRATORY JOURNAL, Vol: 6, Pages: 498-504, ISSN: 0903-1936
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- Citations: 39
JEFFERY PK, 1993, ULTRASTRUCTURE AND IMMUNOHISTOLOGY OF ASTHMA, International Workshop on Rehabilitation of Asthma, Publisher: MUNKSGAARD, Pages: 457-462
Roberts P, Jeffery PK, Mitchell TJ, et al., 1992, Effect of immunization with Freund's adjuvant and pneumolysin on histologic features of pneumococcal infection in the rat lung in vivo., Infect Immun, Vol: 60, Pages: 4969-4972, ISSN: 0019-9567
Immunization with Freund's adjuvant and pneumolysin and stimulation with Freund's adjuvant alone both reduced the severity of the pneumonia caused by injections of bacteria into the apical lobe bronchi of rats. Neither protocol influenced the incidence of pneumococcal bacteremia. Illness sufficiently severe to require sacrifice was delayed from 2.8 days in nonimmunized animals to 5.7 days in those immunized with Freund's adjuvant and pneumolysin (P < 0.05) and 4.5 days in those stimulated with Freund's adjuvant alone (P, not significant).
ROBERTS P, JEFFERY PK, MITCHELL TJ, et al., 1992, EFFECT OF IMMUNIZATION WITH FREUND ADJUVANT AND PNEUMOLYSIN ON HISTOLOGIC FEATURES OF PNEUMOCOCCAL INFECTION IN THE RAT LUNG INVIVO, INFECTION AND IMMUNITY, Vol: 60, Pages: 4969-4972, ISSN: 0019-9567
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- Citations: 7
Read RC, Rutman AA, Jeffery PK, et al., 1992, Interaction of capsulate Haemophilus influenzae with human airway mucosa in vitro., Infect Immun, Vol: 60, Pages: 3244-3252, ISSN: 0019-9567
Two pairs of isogenic capsulate and noncapsulate and one pair of capsulate fimbriate and nonfimbriate strains of Haemophilus influenzae type b were studied in an organ culture of human respiratory mucosa. Over 24 h, the numbers of recovered bacteria increased from the original inoculum size of 10(5) to 10(8) CFU/ml. Transmission electron microscopy and scanning electron microscopy showed that noncapsulate organisms caused significant epithelial damage, whereas capsulate strains did not. Association of noncapsulate bacteria with damaged epithelial cells was observed by 14 h of incubation. In contrast, capsulate organisms were associated with a dense, thick, gel-like matrix which was observed above the epithelial surface. These capsulate organisms were not seen to associate with the epithelial surface (by transmission electron microscopy), though they were occasionally seen adhering to cells by scanning electron microscopy. Fimbriate capsulate H. influenzae showed increased adherence to buccal cells compared with nonfimbriate capsulate organisms. There was also association of fimbriate capsulate bacteria with damaged organ culture epithelium in one of four experiments. It is concluded that both capsule and fimbriae affect the interaction of H. influenzae with human airway mucosa in vitro by influencing adherence to and damage of the epithelium.
READ RC, RUTMAN AA, JEFFERY PK, et al., 1992, INTERACTION OF CAPSULATE HAEMOPHILUS-INFLUENZAE WITH HUMAN AIRWAY MUCOSA INVITRO, INFECTION AND IMMUNITY, Vol: 60, Pages: 3244-3252, ISSN: 0019-9567
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- Citations: 32
Bentley AM, Menz G, Storz C, et al., 1992, Identification of T lymphocytes, macrophages, and activated eosinophils in the bronchial mucosa in intrinsic asthma. Relationship to symptoms and bronchial responsiveness., Am Rev Respir Dis, Vol: 146, Pages: 500-506, ISSN: 0003-0805
Using immunohistochemistry and a panel of monoclonal antibodies, we have compared T-lymphocyte, eosinophil, macrophage, and neutrophil infiltration in bronchial biopsies from 10 intrinsic (nonallergic) asthmatics (IA) and seven extrinsic (allergic) asthmatic (EA), with similar degrees of disease severity. The results were compared with 12 normal healthy nonatopic controls (NC). All subjects were nonsmokers and were not taking oral or inhaled corticosteroids. An intense mononuclear cell infiltrate was identified in IA with an increase in the number of CD45+ cells (total leukocytes), CD3+ and CD4+ lymphocytes, and CD68+ macrophages (p < 0.03, p < 0.01, p < 0.03, and p < 0.03, respectively), compared with NC. Increases were also found in CD4+ (p < 0.05) and CD68+ (p < 0.05) cell numbers between IA and EA. IL-2 receptor-bearing cells (CD25+) and the number of total (MBP+) and actively secreting (EG2+) eosinophils, were also increased in IA compared with NC (p < 0.01, p < 0.01, and p < 0.01, respectively). Similar increases in EG2+ eosinophils and CD25+ (IL-2 receptor-positive) cells were observed in EA (p < 0.01 and p < 0.02, respectively). No differences were detected in the three groups for the number of elastase-positive cells (neutrophils). EG2+ numbers in IA correlated with the Aas asthma symptoms score (r = 0.65, p < 0.05), whereas EG2+ cell numbers in all asthmatics (IA + EA) correlated with airway methacholine responsiveness (r = -0.55, p < 0.03) and with the Aas asthma symptom score (r = 0.54, p < 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)
AZZAWI M, JOHNSTON PW, MAJUMDAR S, et al., 1992, LYMPHOCYTES-T AND ACTIVATED EOSINOPHILS IN AIRWAY MUCOSA IN FATAL ASTHMA AND CYSTIC-FIBROSIS, AMERICAN REVIEW OF RESPIRATORY DISEASE, Vol: 145, Pages: 1477-1482, ISSN: 0003-0805
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- Citations: 162
Feldman C, Read R, Rutman A, et al., 1992, The interaction of Streptococcus pneumoniae with intact human respiratory mucosa in vitro., Eur Respir J, Vol: 5, Pages: 576-583, ISSN: 0903-1936
The interaction of Streptococcus pneumoniae with human ciliated upper respiratory mucosa was studied in an agar-embedded organ culture of nasal turbinate tissue, which only exposed the intact epithelial surface and its secretion. The ciliary beat frequency, measured along the edge of the organ culture, was slowed by 13% in the presence of S. pneumoniae after 16 h (p less than 0.05) compared with the control, and by 24% after 24 h (p less than 0.01). Light microscopy showed bacteria in a thickened gelatinous layer, which obscured the surface of the organ culture. Transmission and scanning electron microscopy confirmed the association of bacteria with the gelatinous layer above an epithelial surface which showed only minor changes compared to uninfected control organ cultures. Contact between bacteria and normal or damaged epithelial cells was not seen. S. pneumoniae in organ culture developed projections from their surface, which were not present after broth culture. S. pneumoniae interactions with epithelial-derived secretions, the formation of a thickened gelatinous layer, and the effects of bacterial toxins on ciliary motility, may be important during colonization of the respiratory tract.
Jeffery PK, Godfrey RW, Adelroth E, et al., 1992, Effects of treatment on airway inflammation and thickening of basement membrane reticular collagen in asthma. A quantitative light and electron microscopic study., Am Rev Respir Dis, Vol: 145, Pages: 890-899, ISSN: 0003-0805
We have obtained airway mucosal biopsies by fiberoptic bronchoscopy for light and electron microscopic analysis of three distinct airway levels of the left lung in three subject groups. Group A: 11 subjects with mild atopic asthma (mean age, 29 yr; %FEV1, 89 to 116%; mean PC20 histamine, 2.42 mg/ml), each biopsied twice, one prior to 4 wk of treatment with either inhaled terbutaline (250 micrograms, two puffs four times daily; n = 5) or inhaled budesonide (200 micrograms, one puff twice daily; n = 6) followed by a second biopsy to allow determination of the effects of treatment. Group B: 10 subjects with severe asthma receiving long-term (average, 3.7 yr) corticosteroid treatment were biopsied once only (mean age, 28 yr; %FEV1, 86 to 129%; mean PC20 histamine, 1.85 mg/ml). Group C: 12 normal healthy control subjects (mean age, 35 yr; %FEV1, 92 to 135%; PC20 histamine greater than 16 mg/ml) biopsied once. By light microscopy of plastic-embedded sections, Group A asthmatics had an increased cellular infiltrate when compared with either the healthy control group or the Group B asthmatics (p less than 0.05). Both asthma groups had a thickening of basement membrane reticular collagen compared with the healthy control group (p less than 0.01). Compared with the control group, there was an increase in the percentage of the total cells that were mast cells (p less than 0.01) and eosinophils (p less than 0.05) in Group A and of eosinophils (p less than 0.01) and histiocytes (p less than 0.01) in Group B. The results of cell counts by electron microscopy largely supported these findings, and, in addition, they demonstrated an increased frequency of foci of free eosinophil granules and decreased numbers of neutrophils (p less than 0.01). By light microscopy, budesonide reduced the percentage of mast cells and eosinophils (p less than 0.05). But for the percentage of lymphocytes, which increased (p less than 0.05), terbutaline was without effect.(ABSTRACT TRUNCATED AT 250 WORDS
Bentley AM, Maestrelli P, Saetta M, et al., 1992, Activated T-lymphocytes and eosinophils in the bronchial mucosa in isocyanate-induced asthma., J Allergy Clin Immunol, Vol: 89, Pages: 821-829, ISSN: 0091-6749
We have studied the phenotype and activation status of leukocytes in the bronchial mucosa in patients with isocyanate-induced asthma. Fiberoptic bronchial biopsy specimens were obtained from nine subjects with occupational (five toluene- and four methylene diisocyanate-sensitive) asthma, 10 subjects with extrinsic asthma, and 12 nonatopic healthy control subjects. Bronchial biopsy specimens were examined by immunohistology with a panel of monoclonal antibodies and the alkaline phosphatase-antialkaline phosphatase method. There was a significant increase in the number of CD25+ cells (interleukin-2 receptor-bearing cells, presumed "activated" T-lymphocytes; p less than 0.01) in isocyanate-induced asthma compared with that of control subjects. There were also significant increases in major basic protein (BMK-13)-positive (p less than 0.02) and EG2-positive (p less than 0.01) cells that represent total and "activated" eosinophil cationic protein-secreting eosinophils, respectively. In agreement with our previous findings, CD25+ (p less than 0.01), BMK-13 (p less than 0.03), and EG2+ (p less than 0.01) cells were also elevated in extrinsic asthma. No significant differences were observed in the numbers of T-lymphocyte phenotypic markers (CD3, CD4, and CD8) between subjects with asthma (isocyanate-induced and extrinsic) and control subjects. Similarly, no significant differences in immunostaining for neutrophil elastase (neutrophils) or CD68 (macrophages) were observed. The results suggest that isocyanate-induced occupational asthma and atopic (extrinsic) asthma have a similar pattern of inflammatory cell infiltrate. The results support the view that T-lymphocyte activation and eosinophil recruitment may be important in asthma of diverse etiology.
GODFREY RWA, SEVERS NJ, JEFFERY PK, 1992, FREEZE-FRACTURE MORPHOLOGY AND QUANTIFICATION OF HUMAN BRONCHIAL EPITHELIAL TIGHT JUNCTIONS, AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, Vol: 6, Pages: 453-458, ISSN: 1044-1549
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- Citations: 23
JEFFERY PK, GODFREY RW, ADELROTH E, et al., 1992, EFFECTS OF TREATMENT ON AIRWAY INFLAMMATION AND THICKENING OF BASEMENT-MEMBRANE RETICULAR COLLAGEN IN ASTHMA - A QUANTITATIVE LIGHT AND ELECTRON-MICROSCOPIC STUDY, AMERICAN REVIEW OF RESPIRATORY DISEASE, Vol: 145, Pages: 890-899, ISSN: 0003-0805
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- Citations: 506
JEFFERY PK, GAILLARD D, MORET S, 1992, HUMAN AIRWAY SECRETORY-CELLS DURING DEVELOPMENT AND IN MATURE AIRWAY EPITHELIUM, EUROPEAN RESPIRATORY JOURNAL, Vol: 5, Pages: 93-104, ISSN: 0903-1936
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- Citations: 70
Jeffery PK, 1992, Histological features of the airways in asthma and COPD., Respiration, Vol: 59 Suppl 1, Pages: 13-16, ISSN: 0025-7931
Asthma and chronic obstructive pulmonary disease (COPD) are complex conditions with imprecise definitions which make definitive morphological comparisons difficult. Broadly, the airways in asthma are occluded by tenacious plugs of exudate and mucus, there is fragility of airway surface epithelium, thickening of the reticular layer beneath the epithelial basal lamina and bronchial vessel congestion and oedema. There is increased inflammatory infiltrate comprising 'activated' lymphocytes and eosinophils with release of granular content in the latter, and there is enlargement of bronchial smooth muscle particularly in medium sized bronchi. Three conditions contribute to COPD. In chronic bronchitis there is mucous hypersecretion with enlargement of tracheo-bronchial submucosal glands and a disproportionate increase of mucous acini. In small (peripheral) airways disease, there is inflammation of bronchioli, mucous metaplasia and hyperplasia, with increased intralumenal mucus, increased wall muscle, fibrosis and airway stenoses. Respiratory bronchiolitis is a critically important early lesion which may predispose to the development of centrilobular emphysema. The severity of destruction of alveolar wall in emphysema appears to be the most important determinant of chronic deterioration of airflow.
Feldman C, Munro NC, Jeffery PK, et al., 1991, Pneumolysin induces the salient histologic features of pneumococcal infection in the rat lung in vivo., Am J Respir Cell Mol Biol, Vol: 5, Pages: 416-423, ISSN: 1044-1549
Streptococcus pneumoniae infections are common, but how they cause host tissue injury and death is incompletely understood. Immunization with pneumolysin, a thiol-activated toxin produced by the pneumococcus, partially protects animals during subsequent infection. The mechanism by which pneumolysin contributes to disease is not known. The aim of the present investigation was to determine the histologic changes induced by recombinant pneumolysin in the rat lung and to compare them with the changes induced by live organisms. Injection of either toxin (200 or 800 ng) or bacteria into the apical lobe bronchus was associated with the development of a severe lobar pneumonia restricted to the apical lobe. The changes induced by the toxin were greater at the higher concentration, and changes were most severe in those animals in which there was partial ligation of the apical lobe bronchus. The pneumonitis was less severe following injection of a modified toxin with decreased hemolytic activity, generated by site-directed mutagenesis of the cloned pneumolysin gene, indicating that this property of the toxin was important in generating pulmonary inflammation. There was still considerable pneumonitis after injection of a modified toxin with decreased capacity to activate complement.
BRADLEY BL, AZZAWI M, JACOBSON M, et al., 1991, EOSINOPHILS, T-LYMPHOCYTES, MAST-CELLS, NEUTROPHILS, AND MACROPHAGES IN BRONCHIAL BIOPSY SPECIMENS FROM ATOPIC SUBJECTS WITH ASTHMA - COMPARISON WITH BIOPSY SPECIMENS FROM ATOPIC SUBJECTS WITHOUT ASTHMA AND NORMAL CONTROL SUBJECTS AND RELATIONSHIP TO BRONCHIAL HYPERRESPONSIVENESS, JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, Vol: 88, Pages: 661-674, ISSN: 0091-6749
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- Citations: 601
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