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Biomedical subjects

E A Kelly

Publications and source records attributed to E A Kelly.

At least 19 recordsLinked to original sources

Cognition, academic progress, behavior and self-concept at 14 years of very low birth weight children.

The aim of this study was to compare cognition, academic progress, behavior, and self-concept children of very low birth weight (VLBW, birth weight < 1501 g) born in the period 1980 to 1982 with randomly selected children of normal birth weight (NBW, birth weight > 2,499 g). At 14 years of age, 130 (84.4%) of 154 VLBW and 42 (70.0%) of 60 NBW children were assessed. Ten VLBW children and one NBW child who had cerebral palsy were excluded. VLBW children scored at a significantly lower level on all three composite scales of the Wechsler Intelligence Scale for Children, 3rd Edition. VLBW children were also significantly disadvantaged on more specific cognitive processes, including tests of visual processing and visual memory and on subtests reflecting learning and problem solving. Only in arithmetic was a difference between the groups discerned on tests of achievement. Significantly more VLBW children were rated by teachers as socially rejected and by their parents as having learning problems at school. VLBW children had significantly reduced self-esteem. VLBW children had more cognitive, academic, and behavioral problems and lower self-esteem at 14 years of age than NBW control subjects.

Achievement↗

Auditory function at 14 years of age of very-low-birthweight.

The aim of the study was to determine audiological function at 14 years of age of very-low-birthweight (VLBW < or = 1500 g) children compared with a cohort of normal birthweight (NBW > 2499 g) children. Participants were consecutive surviving preterm children of birthweight < 1000 g born between 1977 and 1982 (n=86) and of birthweight 1000 to 1500 g born between 1980 and 1982 (n=124) and randomly selected NBW children born between 1981 and 1982 (n=60). Audiometric tests included pure tone audiometry, tympanometry, stapedius muscle reflexes, and measures of central auditory processing. Psychometric tests included measures of IQ, academic achievement, and behaviour. There were no significant differences in rates of hearing impairment, abnormal tympanograms, figure-ground problems, or digit recall between VLBW children and NBW control children. VLBW children had higher rates of some central auditory processing problems, which in turn were associated with poorer intellectual, academic, and behavioural progress.

Adolescent↗

Enhanced cytokine generation by peripheral blood mononuclear cells in allergic and asthma subjects.

BACKGROUND: Although preferential expression of the Th2 cytokines, IL-4 and IL-5, has been described in atopic asthma, the role of IFN-gamma and IL-10 are less clear. OBJECTIVE: To determine the cytokine pattern of T cell mitogen-induced peripheral blood mononuclear cells obtained from atopic asthmatic (AA) subjects. METHODS: Peripheral blood mononuclear cells obtained from AA (n = 24), allergic rhinitis (AR) (n = 9), and normals (NL) (n = 9) were stimulated with phytohemagglutinin (PHA) and the generation of IL-4, IL-5, IFN-gamma, IL-10, and GM-CSF was quantified using ELISA. RESULTS: Compared with NL subjects, peripheral blood mononuclear cells from the atopic groups had increased generation of both IL-5 (AA, P = .001 and AR, P = .024) and IFN-gamma (AA, P = .037 and AR, P = .048) and decreased generation of IL-10 (AA, P = .038 and AR, P = .036). The absolute levels of cytokines did not differ between the two atopic groups; however, the ratio of IL-5/IL-10 was significantly higher in AA (P < .05), but not in AR when compared with NL subjects. CONCLUSION: The concomitant increase in the generation of IL-5 and IFN-gamma, with a decrease in IL-10 in the atopic groups suggests that in, at least a subset of these patients, there is potential expression of both Th2- and Th1-type cytokines. Furthermore, the increased IL-5 to IL-10 ratio could represent a key feature that distinguishes atopic asthmatic from non-asthmatic atopic subjects.

Adolescent↗

Methylxanthines and sensorineural outcome at 14 years in children < 1501 g birthweight.

OBJECTIVES: Methylxanthines, including theophylline, have been used extensively and successfully to treat apnoea in preterm infants. However, long-term consequences of such therapy are largely unknown. The aim of this study was to determine the relationship between theophylline therapy and outcome at 14 years of age in surviving preterm children of birthweight < 1501 g. METHODOLOGY: The subjects of this study were 154 consecutive survivors with birthweights < 1501 g born from 1 October 1980 to 31 March 1982; 130 (84.4%) were assessed at 14 years of age. Outcomes included motor function, psychological test scores, and growth. RESULTS: Of the 130 children assessed, 69 (53.1%) had been exposed to theophylline; 13.0% had cerebral palsy, significantly higher than 1.6% in the 61 children not exposed to theophylline (P < 0.02). This difference remained statistically significant after adjusting for potential confounding variables including the presence of cerebroventricular haemorrhage. In contrast, after adjusting for known confounding variables, children who had received theophylline achieved higher psychological test scores. There was no association between theophylline therapy and growth. CONCLUSIONS: Theophylline therapy in the newborn period is associated with some evidence of harmful, but also helpful sensorineural effects at 14 years of age.

Adolescent↗

The effect of an experimental rhinovirus 16 infection on bronchial lavage neutrophils.

BACKGROUND: Viral respiratory tract infections are the most frequent cause of asthma exacerbations. Of the respiratory viruses associated with these exacerbations, rhinovirus (RV) is the most common. It is proposed that these RV infections may enhance airway inflammation and thus provoke asthma. OBJECTIVE: It is our hypothesis that RV infections generate nasal proinflammatory mediators that are associated with an initial increase in circulating leukocytes and may contribute to later development of neutrophilic airway inflammation. METHODS: To evaluate this hypothesis, subjects with a history of allergic asthma were experimentally inoculated with strain 16 RV (RV16). The effect of this experimental infection was evaluated on circulating leukocytes, nasal-derived mediators, and markers of bronchial inflammation that were obtained by bronchoscopy and lavage. RESULTS: RV16 inoculation was associated with an initial increase in circulating neutrophils. Paralleling these acute changes in circulating neutrophils was an increase in nasal concentrations of IL-8 and granulocyte-colony-stimulating factor (G-CSF). The RV16-associated changes in circulating and nasal G-CSF correlated with increases in peripheral blood neutrophils (r(s) = 0.874, P <. 001 and r(s) = 0.898, P <.001, respectively). Bronchial lavage samples showed no increase in neutrophils 48 hours after RV16 inoculation; however, 96 hours after RV inoculation there was a significant increase in bronchial neutrophils compared with preinoculation values. CONCLUSIONS: These results suggest that the production of nasal mediators associated with the RV infection, particularly G-CSF, may be important to the eventual development of neutrophilic bronchial inflammation and thus contribute to asthma exacerbations.

Adult↗

The relationship of sputum eosinophilia and sputum cell generation of IL-5.

BACKGROUND: Eosinophil recruitment to the airway after antigen challenge is regulated by many factors, including airway cell generation of cytokines. OBJECTIVES: The purpose of this study was to determine the relationship between sputum cell generation of IL-5 and the appearance of eosinophils in the sputum after antigen challenge. METHODS: Sputum samples from 11 allergic subjects were collected before and again 4 and 24 hours after antigen challenge. In 6 of these subjects, induced sputum samples were also obtained 48 hours and 7 days after challenge. Sputum leukocyte differential and cell counts and eosinophil-derived neurotoxin levels were determined. Sputum cells were then cultured with PHA (10 microg/mL) to stimulate IL-5 and IFN-gamma, which were measured in culture supernatants. RESULTS: An increase in sputum eosinophils and eosinophil-derived neurotoxin levels was detected at 4 hours after antigen challenge, with peak values at 24 hours. In contrast, significant increases in ex vivo generation of IL-5 by sputum cells was not seen until 24 hours after challenge. At 24 hours, PHA-induced IL-5 correlated with airspace eosinophil values (r (s) = 0.78, P <.01). In addition, the ratio of IFN-gamma/IL-5 decreased at 24 hours (P <.05) and had an inverse correlation with sputum eosinophils (r (s)= -0.68, P <.05). CONCLUSION: Although eosinophils are increased in the airway lumen as early as 4 hours, the ex vivo generation of IL-5 by sputum cells is first noted in samples obtained 24 hours after antigen challenge. This suggests that the early (4 hours) recruitment of eosinophils to the airway lumen may be regulated by factors other than IL-5 or that mucosal cells (rather than airspace cells) contribute to the IL-5 generation at this time point. Furthermore, IL-5 generation by airspace cells may be more responsible for either eosinophil recruitment or retention at later time points.

Adult↗

Increased matrix metalloproteinase-9 in the airway after allergen challenge.

Persistent asthma is associated with airway inflammation, tissue damage, and deposition of extracellular matrix (ECM) proteins, which may be mediated, in part, through release of matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinase-1 (TIMP-1). To investigate the role of allergen in the induction of MMP-9 and TIMP-1, bronchoscopy and segmental bronchoprovocation (SBP) with saline (SAL) and antigen (AG) were performed in 17 allergic subjects. Bronchoalveolar lavage (BAL) was done 5 min and 48 h after challenge and concentrations of MMP-9 and TIMP-1 in BAL fluid (BALF) were measured by ELISA. Forty-eight hours after AG challenge, concentrations of MMP-9 and TIMP-1 were increased in the airway, but not in serum. Zymography demonstrated that MMP-9 was the predominant metalloproteinase and was present in a latent proform. MMP-9 immunoreactivity was associated primarily with neutrophils, and concentrations of MMP-9 in BALF correlated with airway neutrophils and, to a lesser extent, with alveolar macrophages. These data suggest that AG challenge leads to generation of factors, including MMP-9, that may be associated with the initiation of bronchial injury, which may then lead to remodeling in asthma.

Adult↗

Inhaled budesonide decreases airway inflammatory response to allergen.

To define the mechanisms by which inhaled glucocorticosteroid regulates allergen-induced airway inflammation, a double-blind, placebo-controlled, cross-over study with inhaled budesonide was conducted in 14 subjects with allergic asthma. After baseline bronchoscopy and bronchoalveolar lavage (BAL), subjects were randomized to budesonide (400 microgram, twice daily) or placebo treatment for 4 wk. At the end of each treatment phase, whole-lung allergen inhalation challenge was performed, followed by BAL 48 h later. Budesonide treatment improved the FEV(1), attenuated both the immediate- and late-phase response to allergen, and prevented the increase in bronchial hyperresponsiveness after allergen challenge. Budesonide treatment also decreased allergen-induced airway eosinophilia. To determine the effects of budesonide on airway cell function, BAL cells were stimulated ex vivo with the T cell mitogen PHA, and cytokine generation was measured by ELISA. Budesonide decreased ex vivo generation of IL-5 and IFN-gamma by BAL cells. Ex vivo IL-5 production was significantly correlated with the number of airway eosinophils (r(s) = 0.61), and levels of eosinophil-derived neurotoxin (EDN) (r(s) = 0.57) and IL-5 (r(s) = 0.52) in BAL fluid. Moreover, PHA-induced IL-5 generation correlated with FEV(1) fall during the late-phase response to allergen (r(s) = 0.60). Budesonide decreased circulating eosinophils and serum levels of IL-5, but did not reduce IL-5 generation by peripheral blood mononuclear cells. The reduction in circulating eosinophils correlated with the decrease in levels of EDN (r(s) = 0.61) in BAL fluid and late response to inhaled allergen (r(s) = 0.51). These findings suggest that long-term treatment with inhaled budesonide reduces airway cell generation of cytokines, specifically IL-5, which then decreases circulating eosinophils and their availability for recruitment to the airway after allergen exposure.

Administration, Inhalation↗

Antenatal corticosteroids and outcome at 14 years of age in children with birth weight less than 1501 grams.

OBJECTIVE: To determine whether exposure to antenatal corticosteroid therapy was associated with adverse effects on growth, sensorineural outcome, or lung function of children of birth weight <1501 g at 14 years of age. DESIGN: Cohort study. SETTING: The Royal Women's Hospital, Melbourne, Australia. SUBJECTS: One hundred fifty-four consecutive survivors born from October 1, 1980 to March 31, 1982. INTERVENTIONS: The mothers of 78 survivors (51%) had been given corticosteroids antenatally to accelerate fetal lung maturation. Treatment with antenatal corticosteroids was nonrandom. No mother received >1 course of corticosteroids. OUTCOME MEASURES: The children were assessed at 14 years of age, corrected for prematurity. All assessors were unaware of the exposure of the child to antenatal corticosteroids. The assessments included measurements of growth and neurological, cognitive, and lung function. Growth measurements were converted into z scores (standard deviation) for the appropriate age and gender. RESULTS: Of the 154 survivors, 130 (84%) were assessed at 14 years of age. Overall, the children exposed to antenatal corticosteroids were significantly taller (height z score; mean difference:.39; 95% confidence interval:.001-. 79) and had better cognitive functioning (Wechsler Intelligence Scale for Children-Third Edition Full Scale; IQ mean difference: 6. 2; 95% confidence interval:.8-11.6) than those not exposed to corticosteroids. There were no other differences in sensorineural outcomes between the groups. Lung function was not significantly different between the groups. No conclusions were altered by adjustment for confounding variables. CONCLUSIONS: Exposure to 1 course of antenatal corticosteroid therapy was associated with some clinically and statistically improved outcomes at 14 years of age in children of birth weight <1501 g, with no obvious adverse effects on growth or on sensorineural, cognitive, or lung function. corticosteroids, growth, cognitive, IQ, lung function, adolescence.

Adolescent↗

Segmental antigen challenge increases fibronectin in bronchoalveolar lavage fluid.

Fibronectin may contribute to asthma pathogenesis by recruitment and activation of inflammatory cells, and by promotion of subepithelial fibrosis. Fibronectin is produced by several types of airway cells, including epithelial cells, fibroblasts, and alveolar macrophages. To test the hypothesis that antigen-induced airway inflammation is associated with increased local generation of fibronectin, segmental bronchoprovocation (SBP) with antigen and saline was performed in 17 atopic patients. Bronchoalveolar lavage (BAL) was performed at 5 min and 48 h after segmental challenge with saline or antigen. Fibronectin concentrations in BAL fluid, measured by enzyme-linked immunosorbent assay (ELISA), increased more than 5-fold 48 h after antigen challenge (65 [47 to 110] versus 407 [240 to 697] ng/ml, median and 25 to 75% interquartiles, p < 0.05). Fibronectin concentrations 48 h after antigen challenge correlated with histamine concentrations 5 min after antigen challenge and numbers of eosinophils, neutrophils, macrophages, and total cells in BAL fluid 48 h after antigen challenge. BAL was more enriched in fibronectin 48 h after challenge than would be predicted solely from increased permeability of plasma proteins. Western blot analysis showed that fibronectin in BAL fluid was largely intact and contained the extra domain-A (ED-A) splice variant of cellular fibronectin, indicative of local production. We conclude that antigen challenge in atopic subjects causes increased production of fibronectin by airway cells and speculate that this response may contribute to airway remodeling in allergic inflammation.

Adult↗

Eosinophils bind rhinovirus and activate virus-specific T cells.

Episodes of virus-induced exacerbations of asthma are accompanied by increased eosinophils (EOS) in respiratory secretions and evidence of EOS degranulation. Although rhinoviruses (RV) are the viruses most often implicated in exacerbations of asthma in both children and adults, little is known about the immune response to this group of viruses and, in particular, EOS-RV interactions. To define such interactions, we incubated human rhinovirus type 16 (RV16), a serotype using ICAM-1 as a receptor, with EOS purified from PBMC, and measured EOS-RV binding, EOS-mediated Ag presentation and T cell activation, and EOS cell surface marker expression and superoxide production. Significant RV16 binding occurred to EOS that were pretreated with granulocyte-macrophage CSF, and this binding was inhibited by anti-ICAM-1 mAb. EOS also presented viral Ags to RV16-specific T cells, causing T cell proliferation and secretion of IFN-gamma. RV16 induced a significant shift from CD18dim to CD18bright, but did not affect EOS expression of CD54, CD69, or HLA-DR. Finally, RV16 did not induce superoxide production from peripheral blood EOS. These findings suggest that RV16 also binds to airway EOS, which resemble granulocyte-macrophage CSF-treated blood EOS in terms of high expression of ICAM-1. Furthermore, our findings suggest that EOS could participate in RV-induced immune responses through Ag presentation and T cell activation. By activating RV-specific T cells, EOS may play an important role in the initiation of antiviral T cell responses, and these effects could also contribute to enhanced airway inflammation and increased asthma symptoms in susceptible individuals.

Adult↗

Effect of renal impairment on the pharmacokinetics and tolerability of tiagabine.

PURPOSE: We wished to determine the effect of renal impairment on the pharmacokinetics and tolerability of the new antiepileptic drug tiagabine (TGB). METHODS: We assessed TGB pharmacokinetics and tolerability in 25 subjects with various degrees of renal function (based on creatinine clearance, n = 4-6 per group) from healthy (group I) to requiring hemodialysis (group V) in a single and multiple dose (every 12 h), one-period (groups I-IV) or a single dose, two-period (group V) study (4-mg oral doses of TGB x HCl). Blood samples were collected after the first dose (both periods for group V) and after the last dose on day 5 (groups I-IV). TGB plasma concentrations and plasma protein binding were determined by high-performance liquid chromatography (HPLC) and ultrafiltration, respectively. RESULTS: TGB was well tolerated by all study subjects. The pharmacokinetics of TGB were similar in all subjects; no pharmacokinetic parameter (based on either total or unbound concentrations) was statistically correlated with creatinine clearance. For total TGB in plasma, single-dose mean values of the maximum plasma concentration, clearance, and half-life (t(1/2)) ranged from 52 to 108 ng/ml, from 7.14 to 11.02 l/h, and from 6.4 to 8.4 h, respectively. CONCLUSIONS: TGB pharmacokinetics and tolerability were independent of renal function; therefore, dosage adjustment is unnecessary for epilepsy patients with renal impairment.

Adult↗

Pregnancy outcome after maternal poisoning with brodifacoum, a long-acting warfarin-like rodenticide.

BACKGROUND: Brodifacoum is a potent warfarin-like anticoagulant used in many rat-poisoning products. Its availability has led to several reported human ingestions, none previously reported in pregnancy. CASE: A woman presented at 22 weeks' gestation in hemorrhagic diathesis, attributed to the ingestion of rat poison containing brodifacoum several days earlier. Aggressive vitamin K therapy controlled the maternal coagulopathy, and no fetal hemorrhage was observed by sonography. Her subsequent prenatal course and delivery were unremarkable, and she was delivered of a healthy infant, who has remained well for at least 1 year. CONCLUSION: In this patient, brodifacoum ingestion in pregnancy caused substantial maternal hemorrhage, but no fetal hemorrhage or teratogenic effects were observed.

4-Hydroxycoumarins↗

Rhinovirus-specific T cells recognize both shared and serotype-restricted viral epitopes.

To characterize rhinovirus (RV)-specific T cells, RV16- and RV49-specific CD4 T cells were cloned from peripheral blood, and cytokine secretion and serotype specificity were defined. Each RV-specific clone secreted high levels of interferon-gamma, and several also produced interleukin-4 and -5. To test serotype specificity, each clone was incubated separately with five different RV serotypes. Although 2 of 31 clones proliferated only in response to the virus used in cloning, the rest had significant proliferation in response to 2-5 different serotypes. Thus, RV-specific T cells can be activated by either serotype-specific or shared viral epitopes, raising the possibility that repeated activation of T cells by shared viral determinants in vivo could induce potent recall T cell responses. It is likely that enhanced T cell responses to shared viral epitopes contribute to antiviral activity, airway inflammation, or both.

Antigen-Presenting Cells↗

Cytokine profiles of stimulated blood lymphocytes in asthmatic and healthy adolescents across the school year.

T cell cytokines play an important role in mediating airway inflammation in asthma. The predominance of a Th2 cytokine profile, particularly interleukin (IL)-4 and IL-5, is associated with the pathogenesis and course of asthma. The aim of this study was to test the hypothesis that a stressful life event alters the pattern of cytokine release in asthmatic individuals. Thirteen healthy controls and 21 asthmatic adolescents gave blood samples three times over a semester: midsemester, during the week of final examinations, and 2-3 weeks after examinations. Interferon-gamma (IFN-gamma), IL-2, IL-4, and IL-5 were measured from supernatants of cells stimulated with PHA/PMA for 24 h. Cells from asthmatic subjects released significantly more IL-5 during the examination and postexamination periods, whereas cells from healthy controls released significantly more IL-2 during the midsemester and examination periods, thereby indicating a bias for a Th2-like pattern in asthmatics and a Th1-like pattern in healthy controls. IL-4 and IL-5 production showed a marked decrease during and after examinations in healthy controls, whereas this decline was absent in asthmatics. The ratios of IFN-gamma:IL-4 and IFN-gamma:IL-5 also revealed significant changes in the profile of cytokine release across the semester. These results indicate differential cytokine responses in asthmatics that may become pronounced during periods of cellular activation.

Adolescent↗

The immediate and late allergic response to segmental bronchopulmonary provocation in asthma.

The response to antigen is an important factor in the development of airway inflammation. Segmental bronchoprovocation (SBP) with antigen and subsequent bronchoalveolar lavage (BAL) have provided valuable insight into the mechanisms of allergic inflammation. To determine the features of allergic airway response in asthma, 19 subjects with mild asthma underwent antigen SBP in a dose-dependent manner. The amount of antigen used in SBP was 0 (saline), and 1, 5, or 20% of the antigen dose required to drop the FEV1 by 20% (APD20). BAL was done at 5 min and 48 h after SBP. BAL histamine levels increased modestly 5 min after antigen SBP. At 48 h, there was a marked increase in eosinophils and IL-5 concentration even in airway segments where the release of histamine was small. Moreover, eosinophils correlated with IL-5 levels at 48 h (r = 0.63; p < 0.001), but not with BAL histamine concentrations at 5 min. GM-CSF levels did not increase after antigen SBP and did not correlate with eosinophils. These observations indicate that asthmatic subjects can develop a dose-dependent response to antigen SBP that is characterized by a modest increase in histamine immediately after antigen exposure, and marked eosinophilia, which appears proportionately greater than the histamine response and relatively greater than what is seen in allergic nonasthmatic subjects. This feature might be important to the eventual development of airway inflammation in asthma.

Adult↗

The effect of segmental bronchoprovocation with allergen on airway lymphocyte function.

We hypothesized that allergen-induced airway eosinophilia is linked to activation or recruitment of T cells in the airway and generation of interleukin-5 (IL-5). To evaluate this hypothesis, we performed bronchoscopy with segmental antigen bronchoprovocation in 12 atopic subjects. Bronchoalveolar lavage (BAL) was done 5 min and 48 h after challenge with saline or antigen. Airway cells were isolated and then stimulated ex vivo with a T-cell mitogen, phytohemagglutinin (PHA), and cytokine release was determined. Cells retrieved from the saline-challenged segment secreted principally interferon-gamma (IFN-gamma) and IL-2. In contrast, cells obtained 48 h after allergen challenge secreted high levels of IL-5 and small but increased amounts of IL-4, IL-10, and granulocyte-macrophage colony-stimulating factor (GM-CSF). Although CD4+ T cells were a major source of IL-5, there were no significant changes in the relative proportion of CD4+ cells in response to bronchoprovocation. Additionally, ex vivo secretion of IL-5 by airway cells correlated closely with amounts of IL-5 and eosinophils present in the bronchoalveolar lavage fluid (BALF). These observations suggest that following exposure to allergen, airway T cells are functionally but not phenotypically different from resident airway T cells, and that T cells within the airway contribute to eosinophilic airway inflammation through the secretion of IL-5.

Adult↗

Rhinovirus produces nonspecific activation of lymphocytes through a monocyte-dependent mechanism.

There is evidence that rhinovirus (RV) infections are frequent causes of increased asthmatic symptoms and can specifically enhance allergic inflammation in the airway. To further define effects of RV infection on cellular immunity, we have begun to develop in vitro models for study. When human PBMC were incubated with 35S-labeled RV16, specific binding via ICAM-1 on monocytes was observed. Incubation of PBMC with RV also led to a dose-related increase in the expression of the early activation marker CD69 on 30 to 70% of T cells. The RV16-induced increases in CD69 were blocked by anti-ICAM-1 mAb, and were not elicited by UV-inactivated (noninfectious) virus. The degree of CD69 enhancement correlated with the number of monocytes in mixtures of PBMC, did not occur in monocyte-depleted cultures, and was mediated by one or more soluble factor(s). RV also induced secretion of IFN-gamma from both peripheral blood T cells and NK cells, and IFN-gamma mRNA was greatest in T cells that were CD69+. Finally, supernatant from RV-activated CD3+CD69+ cells had biologic activity that promoted eosinophil survival in vitro; this RV16-associated activity was blocked when co-incubations were performed with IFN-gamma mAbs. These observations suggest that RV nonspecifically activates a large proportion of T cells through a monocyte-dependent mechanism. Such changes in vivo could enhance airway inflammation, and this may include effects on inflammatory cells in the airways of allergic individuals.

Adult↗