Journal articles on the topic '110701 Allergy'
To see the other types of publications on this topic, follow the link: 110701 Allergy.
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 24 journal articles for your research on the topic '110701 Allergy.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.
1
Sicherer, Scott H. "Early introduction of peanut to infants at high allergic risk can reduce peanut allergy at age 5 years." Evidence Based Medicine 20, no. 6 (September 17, 2015): 204. http://dx.doi.org/10.1136/ebmed-2015-110201.
Full text
2
Stayoussef, Mouna, Jihen Benmansour, Fayza A. Al-Jenaidi, Hichem B. Said, Chiheb B. Rayana, Touhami Mahjoub, and Wassim Y. Almawi. "Glutamic Acid Decarboxylase 65 and Islet Cell Antigen 512/IA-2 Autoantibodies in Relation to Human Leukocyte Antigen Class II DR and DQ Alleles and Haplotypes in Type 1 Diabetes Mellitus." Clinical and Vaccine Immunology 18, no. 6 (April 13, 2011): 990–93. http://dx.doi.org/10.1128/cvi.00073-11.
Full textAbstract:
ABSTRACTThe frequencies of autoantibodies against glutamic acid decarboxylase 65 (GAD65) and islet cell antigen (ICA) 512/IA-2 (512/IA-2) are functions of the specific human leukocyte antigen (HLA) in type 1 diabetes mellitus (T1D). We investigated the association of HLA class II (DR and DQ) alleles and haplotypes with the presence of GAD and IA-2 autoantibodies in T1D. Autoantibodies were tested in 88 Tunisian T1D patients and 112 age- and gender-matched normoglycemic control subjects by enzyme immunoassay. Among T1D patients, mean anti-GAD antibody titers were higher in theDRB1*030101allele (P< 0.001), together with theDRB1*030101/DQB1*0201(P< 0.001) andDRB1*040101/DQB1*0302(P= 0.002) haplotypes, while lower anti-GAD titers were associated with theDRB1*070101(P= 0.001) andDRB1*110101(P< 0.001) alleles andDRB1*070101/DQB1*0201(P= 0.001) andDRB1*110101/DQB1*030101(P= 0.001) haplotypes. Mean anti-IA-2 antibody titers were higher in theDRB1*040101allele (P= 0.007) andDRB1*040101/DQB1*0302(P= 0.001) haplotypes but were lower in theDRB1*110101allele (P= 0.010) and theDRB1*110101(P< 0.001) andDRB1*110101/DQB1*030101(P= 0.025) haplotypes. Multinomial regression analysis confirmed the positive association ofDRB1*030101and the negative association ofDRB1*110101andDQB1*030101, along with theDRB1*070101/DQB1*0201andDRB1*110101/DQB1*030101haplotypes, with anti-GAD levels. In contrast, only theDRB1*040101/DQB1*0302haplotype was positively associated with altered anti-IA-2 titers. Increased GAD65 and IA-2 antibody positivity is differentially associated with select HLA class II alleles and haplotypes, confirming the heterogeneous nature of T1D.
3
Almawi, Wassim Y., Marc Busson, Hala Tamim, Einas M. Al-Harbi, Ramzi R. Finan, Saria F. Wakim-Ghorayeb, and Ayesha A. Motala. "HLA Class II Profile and Distribution of HLA-DRB1 and HLA-DQB1 Alleles and Haplotypes among Lebanese and Bahraini Arabs." Clinical Diagnostic Laboratory Immunology 11, no. 4 (July 2004): 770–74. http://dx.doi.org/10.1128/cdli.11.4.770-774.2004.
Full textAbstract:
ABSTRACT The gene frequencies of HLA class II alleles were studied in 95 healthy Lebanese Arab and 72 healthy Bahraini Arab subjects. Our aim was to establish the genetic relationship between Bahraini and Lebanese Arabs in terms of HLA class II gene and haplotype frequencies and to compare these results with frequencies for other countries with populations of Caucasian and non-Caucasian descent. Subjects were unrelated and of both sexes, and HLA-DRB1 and -DQB1 genotyping was done by the PCR sequence-specific primer technique. Comparative analysis of the HLA-DR and -DQ alleles revealed differences in the allelic distribution among Bahraini and Lebanese subjects. Analysis of the 25 HLA-DRB1 alleles that have been investigated showed that the DRB1*040101 and DRB1*110101 alleles were more frequent among Lebanese, whereas DRB1*030101 and DRB1*160101 alleles were more frequent among Bahrainis. Similarly, of the seven HLA-DQB1 alleles analyzed, the presence of DQB1*0201 was more frequent among Bahrainis, whereas DQB1*030101 was more frequent among Lebanese. The DRB1*160101-DQB1*050101 (0.1318 versus 0.0379%) and DRB1*030101-DQB1*0201 (0.1202 versus 0.0321%) haplotypes were more frequent among Bahrainis, while the DRB1*110101-DQB1*030101 (0.3142 versus 0.1198%) and DRB1*040101-DQB1*0302 (0.1416 versus 0.0278%) haplotypes were more frequent in Lebanese subjects. Furthermore, a high prevalence of the DRB1*040101-DRB1*110101-DQB1*0302-DQB1*030101 (12.63 versus 1.35%, P = 0.015) and the homozygous DRB1*110101-DRB1*110101-DQB1*030101-DQB1*030101 (7.37 versus 0.00%, P = 0.046) genotypes was seen among Lebanese, and DRB1*070101-DRB1*160101-DQB1*0201-DQB1*050101 (6.76 versus 0.00%, P = 0.034) was seen more frequently among Bahraini subjects. Our results underline significant differences between these two populations in HLA class II distribution, provide basic information for further studies of major histocompatibility complex heterogeneity among Arabic-speaking countries, and serve as a reference for further anthropological studies.
4
Sharma, Rashmi, Ravi Deval, Vikash Priyadarshi, Shailendra N. Gaur, Ved P. Singh, and Anand B. Singh. "Indoor Fungal Concentration in the Homes of Allergic/Asthmatic Children in Delhi, India." Allergy & Rhinology 2, no. 1 (January 2011): ar.2011.2.0005. http://dx.doi.org/10.2500/ar.2011.2.0005.
Full textAbstract:
Allergy to fungi has been linked to a wide range of illnesses, including rhinitis and asthma. Therefore, exposure to fungi in home environment is an important factor for fungal allergy. The present study was aimed to investigate types of airborne fungi inside and outside the homes of asthmatic children and control subjects (nonasthmatic children). The dominant fungi were evaluated for their quantitative distribution and seasonal variation. The air samples were collected from indoors and immediate outdoors of 77 selected homes of children suffering from bronchial asthma/allergic rhinitis using Andersen volumetric air sampler. The isolated fungal genera/species were identified using reference literature, and statistical analysis of the dominant fungi was performed to study the difference in fungal concentration between indoor and immediate outdoor sites as well as in between different seasons. A total of 4423 air samples were collected from two indoor and immediate outdoor sites in a 1-year survey of 77 homes. This resulted in the isolation of an average of 110,091 and 107,070 fungal colonies per metric cube of air from indoor and outdoor sites, respectively. A total of 68 different molds were identified. Different species of Aspergillus, Alternaria, Cladosporium, and Penicillium were found to be the most prevalent fungi in Delhi homes, which constituted 88.6% of the total colonies indoors. Highest concentration was registered in autumn and winter months. Total as well as dominant fungi displayed statistically significant differences among the four seasons (p < 0.001). The largest number of isolations were the species of Aspergillus ( >40% to total colony-forming units in indoors as well as outdoors) followed by Cladosporium spp. Annual concentration of Aspergillus spp. was significantly higher (p < 0.05) inside the homes when compared with outdoors. Most of the fungi also occurred at a significantly higher (p < 0.001) rate inside the homes when compared with immediate outdoors. Asthmatic children in Delhi are exposed to a substantial concentration of mold inside their homes as well as immediate outdoor air. The considerable seasonal distributions of fungi provide valuable data for investigation of the role of fungal exposure as a risk for respiratory disorders among patients suffering from allergy or asthma in Delhi.
5
Al-Harbi, Einas M., Abdul-Jabbar Abbassi, Hala Tamim, Fayza al-Jenaidi, Mariam Kooheji, Madeeha Kamal, Salwa al-Mahroos, Faisal al-Nasir, Ayesha A. Motala, and Wassim Y. Almawi. "Specific HLA-DRB and -DQB Alleles and Haplotypes Confer Disease Susceptibility or Resistance in Bahraini Type 1 Diabetes Patients." Clinical Diagnostic Laboratory Immunology 11, no. 2 (March 2004): 292–96. http://dx.doi.org/10.1128/cdli.11.2.292-296.2004.
Full textAbstract:
ABSTRACT Insofar as genetic susceptibility to type 1 diabetes is associated with HLA class II genes, with certain allelic combinations conferring disease susceptibility or resistance, this study assessed the distributions of HLA-DR and -DQ among 107 unrelated patients with type 1 diabetes and 88 healthy controls from Bahrain, all of Arab origin. The HLA-DRB and -DQB genotypes were determined by PCR-sequence-specific priming. The following alleles showed the strongest association with type 1 diabetes among patients versus controls according to their frequencies: DRB1*030101 (0.430 versus 0.097; P < 0.001), DRB1*040101 (0.243 versus 0.034; P < 0.001), DQB1*0201 (0.467 versus 0.193; P < 0.001), and DQB1*0302 (0.229 versus 0.091; P < 0.001). When the frequencies of alleles in controls were compared to those in patients, negative associations were seen for DRB1*100101 (0.085 versus 0.014; P < 0.001), DRB1*110101 (0.210 versus 0.060; P < 0.001), DQB1*030101 (0.170 versus 0.075; P = 0.006), and DQB1*050101 (0.335 versus 0.121; P < 0.001). In addition, the DRB1*030101-DQB1*0201 (70.1 versus 22.7%; P < 0.001) and DRB1*030101-DQB1*0302 (21.5 versus 0.0%; P < 0.001) genotypes were more prevalent among patients, thereby conferring disease susceptibility, whereas the DRB1*100101-DQB1*050101 (20.5 versus 2.8%; P < 0.001), DRB1*110101-DQB1*030101 (28.4 versus 8.4%; P < 0.001), and DRB1*110101-DQB1*050101 (30.7 versus 0.9%; P < 0.001) genotypes were more prevalent among controls, thus assigning a protective role. These results confirm the association of specific HLA-DR and -DQ alleles and haplotypes with type 1 diabetes and may underline several characteristics that distinguish Bahraini patients from other Caucasians patients.
6
Almawi, Wassim Y., Saria F. Wakim-Ghorayeb, Mona R. Arekat, Pierre Najm, Sose H. Keleshian, Nasreen Al-Sayed, Bruno Blanchon, Hanady R. Samaha, and Noha Irani-Hakime. "Association of Selective HLA Class II Susceptibility-Conferring and Protective Haplotypes with Type 2 Diabetes in Patients from Bahrain and Lebanon." Clinical and Vaccine Immunology 13, no. 11 (September 20, 2006): 1296–98. http://dx.doi.org/10.1128/cvi.00206-06.
Full textAbstract:
ABSTRACT The association of HLA class II with type 2 diabetes (T2DM) was investigated in Bahraini and Lebanese subjects. DRB1*070101 (Lebanese and Bahraini) and DQB1*0201 (Lebanese) were susceptibility-conferring alleles, and unique susceptibility-conferring/protective haplotypes were found in both patient groups. Regression analysis confirmed that DRB1*070101-DQB1*0201 (Bahraini) and DRB1*110101-DQB1*0201 (Lebanese) were susceptibility-conferring haplotypes.
7
BOOKMAN, ARTHUR. "Imaging of Arthritis and Metabolic Bone Disease." Journal of Rheumatology 38, no. 5 (May 2011): 968.1–968. http://dx.doi.org/10.3899/jrheum.110001.
Full text
8
SHARIF, ROOZBEH, MARVIN J. FRITZLER, MAUREEN D. MAYES, EMILIO B. GONZALEZ, TERRY A. McNEARNEY, HILDA DRAEGER, MURRAY BARON, et al. "Anti-Fibrillarin Antibody in African American Patients with Systemic Sclerosis: Immunogenetics, Clinical Features, and Survival Analysis." Journal of Rheumatology 38, no. 8 (May 15, 2011): 1622–30. http://dx.doi.org/10.3899/jrheum.110071.
Full textAbstract:
Objective.Anti-U3-RNP, or anti-fibrillarin antibodies (AFA), are detected more frequently among African American (AA) patients with systemic sclerosis (SSc) compared to other ethnic groups and are associated with distinct clinical features. We examined the immunogenetic, clinical, and survival correlates of AFA in a large group of AA patients with SSc.Methods.Overall, 278 AA patients with SSc and 328 unaffected AA controls were enrolled from 3 North American cohorts. Clinical features, autoantibody profile, and HLA class II genotyping were determined. To compare clinical manifestations, relevant clinical features were adjusted for disease duration. Cox proportional hazards regression was used to determine the effect of AFA on survival.Results.Fifty (18.5%) AA patients had AFA. After Bonferroni correction, HLA-DRB1*08:04 was associated with AFA, compared to unaffected AA controls (OR 11.5, p < 0.0001) and AFA-negative SSc patients (OR 5.2, p = 0.0002). AFA-positive AA patients had younger age of disease onset, higher frequency of digital ulcers, diarrhea, pericarditis, higher Medsger perivascular and lower Medsger lung severity indices (p = 0.004, p = 0.014, p = 0.019, p = 0.092, p = 0.006, and p = 0.016, respectively). After adjustment for age at enrollment, AFA-positive patients did not have different survival compared to patients without AFA (p = 0.493).Conclusion.Our findings demonstrate strong association between AFA and HLA-DRB1*08:04 allele in AA patients with SSc. AA SSc patients with AFA had younger age of onset, higher frequency of digital ulcers, pericarditis and severe lower gastrointestinal involvement, but less severe lung involvement compared to AA patients without AFA. Presence of AFA did not change survival.
9
BINGHAM, CLIFTON O., RIEKE ALTEN, SUSAN J. BARTLETT, VIVIAN P. BYKERK, PETER M. BROOKS, ERNEST CHOY, ROBIN CHRISTENSEN, et al. "Identifying Preliminary Domains to Detect and Measure Rheumatoid Arthritis Flares: Report of the OMERACT 10 RA Flare Workshop." Journal of Rheumatology 38, no. 8 (August 2011): 1751–58. http://dx.doi.org/10.3899/jrheum.110401.
Full textAbstract:
Background.While disease flares in rheumatoid arthritis (RA) are a recognized aspect of the disease process, there is limited formative research to describe them.Methods.The Outcome Measures in Rheumatology Clinical Trials (OMERACT) RA Flare Definition Working Group is conducting an international research project to understand the specific characteristics and impact of episodic disease worsening, or “flare,” so that outcome measures can be developed or modified to reflect this uncommonly measured, but very real and sometimes disabling RA disease feature. Patient research partners provided critical insights into the multidimensional nature of flare. The perspectives of patients and healthcare and research professionals are being integrated to ensure that any outcome measurement to detect flares fulfills the first OMERACT criteria of Truth. Through an iterative data-driven Delphi process, a preliminary list of key domains has been identified to evaluate flare.Results.At OMERACT 10, consensus was achieved identifying features of flare in addition to the existing core set for RA, including fatigue, stiffness, symptom persistence, systemic features, and participation. Patient self-report of flare was identified as a component of the research agenda needed to establish criterion validity for a flare definition; this can be used in prospective studies to further evaluate the Discrimination and Feasibility components of the OMERACT filter for a flare outcome measure.Conclusion.Our work to date has provided better understanding of key aspects of the RA disease process as episodic, potentially disabling disease worsening even when a patient is in low disease activity. It also highlights the importance of developing ways to enhance communication between patients and clinicians and improve the ability to achieve “tight control” of disease.
10
Mahdi, Najat, Khadija Al-Ola, Abeer M. Al-Subaie, Muhallab E. Ali, Zaid Al-Irhayim, A. Qader Al-Irhayim, and Wassim Y. Almawi. "HLA Class II Haplotypes Distinctly Associated with Vaso-Occlusion in Children with Sickle Cell Disease." Clinical and Vaccine Immunology 15, no. 4 (February 13, 2008): 729–31. http://dx.doi.org/10.1128/cvi.00425-07.
Full textAbstract:
ABSTRACT We investigated the association of HLA class II alleles and haplotypes with sickle cell anemia vaso-occlusive crisis (VOC). DRB1*100101 was positively associated, while DRB1*140101, DRB1*150101, and DQB1*060101 were negatively associated, with VOC. Both susceptible (DRB1*100101-DQB1*050101) and protective (DRB1*110101-DQB1*030101 and DRB1*150101-DQB1*060101) haplotypes were identified, indicating that HLA class II haplotypes influence VOC risk.
11
Stayoussef, Mouna, Jihen Benmansour, Abdul-Qader Al-Irhayim, Hichem B. Said, Chiheb B. Rayana, Touhami Mahjoub, and Wassim Y. Almawi. "Autoimmune Type 1 Diabetes Genetic Susceptibility Encoded by Human Leukocyte Antigen DRB1 and DQB1 Genes in Tunisia." Clinical and Vaccine Immunology 16, no. 8 (June 24, 2009): 1146–50. http://dx.doi.org/10.1128/cvi.00105-09.
Full textAbstract:
ABSTRACT Human leukocyte antigen (HLA) class II genes contribute to the genetic susceptibility to type 1 diabetes (T1D), and susceptible alleles and haplotypes were implicated in the pathogenesis of T1D. This study investigated the heterogeneity in HLA class II haplotype distribution among Tunisian patients with T1D. This was a retrospective case control study done in Monastir in central Tunisia. The subjects comprised 88 T1D patients and 112 healthy controls. HLA-DRB1 and -DQB1 genotyping was done by PCR-sequence-specific priming. Significant DRB1 and DQB1 allelic differences were seen between T1D patients and controls; these differences comprised DRB1*030101 and DQB1*0302, which were higher in T1D patients than in control subjects, and DRB1*070101, DRB1*110101, DQB1*030101, and DQB1*060101, which were lower in T1D patients than in control subjects. In addition, the frequencies of DRB1*030101-DQB1*0201 and DRB1*040101-DQB1*0302 were higher in T1D patients than in control subjects, and the frequencies of DRB1*070101-DQB1*0201 and DRB1*110101-DQB1*030101 haplotypes were lower in T1D patients than in control subjects. Multiple logistic regression analysis revealed the positive association of DRB1*030101-DQB1*0201 and DRB1*040101-DQB1*0302 and the negative association of only DRB1*070101-DQB1*0201 haplotypes with T1D. Furthermore, a significantly increased prevalence of DRB1*030101-DQB1*0201 homozygotes was seen for T1D subjects than for control subjects. Our results confirm the association of specific HLA-DR and -DQ alleles and haplotypes with T1D in Tunisians. The identification of similar and unique haplotypes in Tunisians compared to other Caucasians highlights the need for evaluating the contribution of HLA class II to the genetic susceptibility to T1D with regard to haplotype usage and also to ethnic origin and racial background.
12
D'Souza, Shaina J., Vicki Immethun, Matthew Godwin, and James B. McLachlan. "Sexual dimorphism in the antigen-specific T cell response in S. Typhimurium infections within extra-lymphoid tissues." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 110.01. http://dx.doi.org/10.4049/jimmunol.208.supp.110.01.
Full textAbstract:
Abstract Differences in susceptibility to and severity of infectious diseases between the sexes are well established. Females often generate a beneficially stronger immune response when combatting infection but show an increased risk of developing autoimmunity. While the sex-related hormone estradiol is known to affect CD4 T cell cytokine release in vitro, less is known about T cells behavior in vivo. To address this, we intravenously infected male and female mice with attenuated Salmonella Typhimurium (S. Tm). By day 15 post infection (p.i.), male mice showed significantly lower rates of survival. Males also generated a higher number of S. Tm-specific CD4 T cells in the liver but, conversely, displayed higher bacterial burdens. To isolate the role of sex hormones, mice were gonadectomized before reaching sexual maturity and then infected. Ovariectomized mice lost significantly more weight than ovary-intact females by day 15 p.i. Like normal males, ovariectomized females demonstrated a significantly higher number of S. Tm-specific CD4 T cells but also higher liver bacterial burdens. To investigate the role of extra-lymphoid tissues such as the liver, we infected lymphotoxin-alpha (LTa) mice that genetically lack lymphoid tissues. Surprisingly, we found the stark difference in survival and CD4 T cell expansion between the sexes was lost. These differences in T cell expansion, and the commensurate effect on survival, in the presence or absence of endogenous sex hormones or lymphoid tissues indicate that females may have evolved a separate ability to regulate immune responses outside of traditional lymphoid organs. These studies will provide insights into sex-based differences seen in cellular immunity against bacterial pathogens in vivo. Supported by a grant from the Keck Foundation
13
D’cruz, D., G. Eriksson, Y. Green, A. Hammer, B. Ji, P. Meizlik, and D. Roth. "POS0696 SAFETY AND EFFICACY OF BELIMUMAB IN OLDER ADULTS WITH SYSTEMIC LUPUS ERYTHEMATOSUS: RESULTS OF AN INTEGRATED ANALYSIS." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 596.1–596. http://dx.doi.org/10.1136/annrheumdis-2021-eular.2217.
Full textAbstract:
Background:Systemic lupus erythematosus (SLE) is a chronic, autoimmune disease characterised by persistent B-cell activation. Belimumab (BEL), a monoclonal antibody that inhibits B-lymphocyte stimulator, is approved in patients aged ≥5 years with active autoantibody-positive SLE; however, safety and efficacy data of BEL in older adults are limited.Objectives:Assess the safety and efficacy of BEL in older adults with SLE.Methods:A meta-analysis (GSK study 116559) was performed on the subpopulation of patients aged ≥65 years and compared with the overall population pooled from six controlled, repeat-dose (CRD) BEL trials in adults with SLE (GSK studies: 110752, 110751, LBSL02 [safety only], 112341, 113750, and 115471). Additional safety data were obtained from GSK study 115467.In each trial, patients were randomised to BEL or placebo (PBO) and received ≥1 treatment dose (GSK studies 110752 and 110751: intravenous [IV] BEL 1 or 10 mg/kg; LBSL02: IV BEL 1, 4, or 10 mg/kg; GSK study 112341: subcutaneous BEL 200 mg; GSK studies 113750, 115471, and 115467: IV BEL 10 mg/kg) plus standard therapy. Safety assessments included: incidence of serious adverse events (SAE), mortality and adverse events of special interest (AESI). The primary efficacy analysis for the CRD trials was the SLE Responder Index 4 (SRI4) response rate.Results:Older adults (CRD studies: N=63; study 115467: N=156) had lower disease activity and more organ damage compared with the overall populations, and a greater proportion were of white race compared with the overall population in the CRD studies. There were no clinically relevant differences in the incidence of SAE or death between older adults and the overall populations (Table 1). Rates of AESI (post-infusion/injection systemic reactions [PISR], serious infections of special interest, malignancies, psychiatric events) were generally similar or lower in older adults compared with the overall populations with no imbalances between BEL and PBO in older adults (Table 1). No malignancies were reported in older adults. The SRI4 response rate in older adults favoured BEL vs PBO (OR [95% CI], 1.49 [0.49, 4.58]), consistent with the overall populations of the individual CRD studies (110752 and 110751 pooled [10 mg/kg IV]: 1.68 [1.32, 2.15]; 112341: 1.68 [1.25, 2.25]; 113750: 1.99 [1.40, 2.82]; 115471: 1.42 [0.94, 2.15]).Conclusion:In patients with SLE, the safety and efficacy of BEL in older adults were generally consistent with the overall population and suggest a favourable benefit–risk profile. Due to the small number of older adults analysed, these data should be interpreted with caution.Funding:GSKTable 1.SAE, deaths, and AESIN (%)*Study 115467CRD studies†Older adults(N=156)Overall(N=4003)Older adults(N=63)Overall(N=4170)PBON=82BELN=74PBON=2001BELN=2002PBON=27BELN=36PBON=1355BELN=2815SAE9 (11.0)6 (8.1)222 (11.1)220 (11.0)5 (18.5)10 (27.8)230 (17.0)421 (15.0)Death‡1 (1.2)1 (1.4)11 (0.5)12 (0.6)006 (0.4)16 (0.6)AESI PISR§,‖,¶----02 (5.6)110 (8.1)286 (10.2) Serious PISR002 (<0.1)8 (0.4)002 (0.1)13 (0.5)Infections of SI (opportunistic, herpes zoster, tuberculosis, sepsis)§02 (2.7)50 (2.5)36 (1.8)1 (3.7)097 (7.2)173 (6.1)Serious infections of SI02 (2.7)17 (0.8)17 (0.8)0017 (1.3)40 (1.4)Malignancies ex. non-melanoma skin cancer§005 (0.2)5 (0.2)002 (0.1)8 (0.3)Depression(inc. mood disorders /anxiety)/suicide/self-injury§,¶,**-‖---3 (11.1)3 (8.3)92 (6.8)210 (7.5)Serious depression/ suicide/self-injury01 (1.4)6 (0.3)18 (0.9)1 (3.7)05 (0.4)9 (0.3)*Patients counted once/category; †Pooled data from all studies except 115467; ‡Study 115467: fatal SAEs that started during on-treatment period; death may have occurred after period end. CRD studies: all deaths during double-blind period; §Per custom MedDRA query; ‖Occurring on/within 3 days of infusion/injection; ¶Study 115467: only serious PISR and serious depression/suicide/self-injury events collected; **Per standard MedDRA query.MedDRA, Medical Dictionary for Regulatory Activities; SI, special interestAcknowledgements:Medical writing assistance was provided by Helen Taylor, Fishawack Indicia Ltd., UK, part of Fishawack Health, and was funded by GSK.Disclosure of Interests:David d’cruz Speakers bureau: GSK, Consultant of: GSK, Eli Lilly, Gina Eriksson Shareholder of: GSK, Employee of: GSK, Yulia Green Shareholder of: GSK, Employee of: GSK, Anne Hammer Shareholder of: GSK, Employee of: GSK, Beulah Ji Shareholder of: GSK, Employee of: GSK, Paige Meizlik Shareholder of: GSK, Employee of: GSK, David Roth Shareholder of: GSK, Employee of: GSK
14
Busca, Aurelia, and Ashok Kumar. "Macrophages differentiation confers resistance to HIV-Vpr induced apoptosis (110.10)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 110.10. http://dx.doi.org/10.4049/jimmunol.186.supp.110.10.
Full textAbstract:
Abstract Macrophages represent major viral reservoirs during HIV infection, because they are long lived and resistant to HIV cytopathic effects. We have evaluated the role of Bcl2 and IAPs (inhibitors of apoptosis), the main families of antiapoptotic proteins, in macrophage resistance during HIV infection by using the HIV accessory protein Vpr as a study model for apoptosis. Our results show that human monocytes are sensitive to Vpr but develop resistance following differentiation into macrophages. Vpr efficiently down-regulated cIAP1 and Bcl2 in sensitive monocytes but not in macrophages, suggesting that these molecules could be implicated in the enhanced resistance of macrophages to HIV-Vpr apoptosis. However, Bcl2 inactivation with the HA14-1 inhibitor was able to induce cell death on its own, with no impact on susceptibility to Vpr apoptosis. By using siRNA to knock down the expression of IAP1 and IAP2 proteins and SMAC mimetic to induce their degradation, macrophages could be sensitized to Vpr-induced cell death. Our results suggest that IAPs and not Bcl2 family confer a resistant phenotype that is relevant for macrophage survival in the context of HIV infection. Modulation of the apoptotic pathway during monocyte differentiation provides insight into the possible mechanisms for viral reservoirs persistence in macrophages and into potential therapeutic approaches to target antiapoptotic genes.
15
Motala, Ayesha A., Marc Busson, Einas M. Al-Harbi, Manal A. A. Khuzam, Emtiaz M. D. Al-Omari, Mona R. Arekat, and Wassim Y. Almawi. "Susceptible and Protective Human Leukocyte Antigen Class II Alleles and Haplotypes in Bahraini Type 2 (Non-Insulin-Dependent) Diabetes Mellitus Patients." Clinical Diagnostic Laboratory Immunology 12, no. 1 (January 2005): 213–17. http://dx.doi.org/10.1128/cdli.12.1.213-217.2005.
Full textAbstract:
ABSTRACT Whereas the genetic risk for type 1 diabetes is linked to human leukocyte antigen (HLA) class II genes, the HLA association in type 2 (non-insulin-dependent) diabetes is less clear. The association between HLA class II genotypes and type 2 diabetes was examined in adult Bahrainis, an Arab population with a high prevalence of type 2 diabetes. HLA-DRB1* and -DQB1* genotyping of 86 unrelated type 2 diabetes patients (age, 51.6 ± 8.2 years; mean duration of diabetes, 7.7 ± 7.1 years) who had a strong family history of diabetes (52 of 72 versus 0 of 89 for controls, P < 0.001) and 89 healthy subjects was done by PCR-sequence-specific priming. DRB1*040101 (0.1221 versus 0.0562, P = 0.019) and DRB1*070101 (0.2151 versus 0.0843, P < 0.001) were positively associated, while DRB1*110101 (0.0698 versus 0.1461, P = 0.014) and DRB1*160101 (0.0640 versus 0.1236, P = 0.038) were negatively associated with type 2 diabetes. DRB1*040101-DQB1*0302 (0.069 versus 0.0007; P = 0.004), DRB1*070101-DQB1*0201 (0.178 versus 0.0761, P = 0.007), DRB1*070101-DQB1*050101 (0.125 versus 0.0310, P = 0.002), and DRB1*150101-DQB1*060101 (0.0756 versus 0.0281, P = 0.008) were more prevalent among patients, while DRB1*160101-DQB1*050101 (0.0702 versus 0.0349, P = 0.05) was more prevalent among controls, conferring disease susceptibility or protection, respectively. In Bahrainis with type 2 diabetes, there is a significant association with select HLA class II genotypes, which were distinct from those in type 1 diabetes.
16
Parameswaran, Narayanan, Babu Gonipeta, Sitaram Parvataneni, Nandakumar Packiriswamy, and Deepika Sharma. "β-arrestin-1 negatively regulates inflammatory response to polymicrobial sepsis in mice (110.11)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 110.11. http://dx.doi.org/10.4049/jimmunol.186.supp.110.11.
Full textAbstract:
Abstract β-arrestins are scaffolding proteins that regulate a number of receptor signaling pathways including Toll-like receptors. We recently demonstrated that mice lacking either β-arrestin-1 or β-arrestin-2 are protected from lipopolysaccharide-induced lethality and have a markedly reduced inflammatory response. To assess the role of β-arrestin-1 in a clinically relevant model of sepsis, we subjected wild type and β-arrestin-1 knockout mice to cecal-ligation and puncture (CLP) to mimick septic peritonitis and polymicrobial sepsis. Surprisingly, we found that, mortality of β-arrestin-1 knockout mice was significantly enhanced compared to the wild type mice after CLP. Consistent with lethality, β-arrestin-1 knockout mice had markedly elevated inflammatory cytokine levels in the plasma, peritoneal cavity, and bronchoalveolar fluid. Enhanced systemic inflammatory response of β-arrestin-1 knockout mice was associated with significantly enhanced infiltration of immune cells into the peritoneal cavity after induction of septic peritonitis. Together, these results demonstrate that, contrary to its role in lipolysaccharide-TLR4 signaling in vivo, β-arrestin-1 is a negative regulator of inflammation induced by polymicrobial sepsis and that the phenotype of the mice may be related to a potentially aberrant immune response from excess infiltration of immune cells. These results also suggest that the role of β-arrestin-1 in this model is likely independent of its role in TLR4 signaling in vivo.
17
McLane, Laura, Gabriela Cosma, Michael Paley, E. Wherry, George Makedonas, and Michael Betts. "Differential localization of T-bet and Eomes within distinct human CD8 T-cell memory populations (110.10)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 110.10. http://dx.doi.org/10.4049/jimmunol.188.supp.110.10.
Full textAbstract:
Abstract In mice, two T-box transcription factors, T-bet and Eomes, drive the differentiation of CD8 T-cell lineages; however, little is known regarding their role in human CD8 T-cell differentiation. Here, we characterized T-bet and Eomes expression and localization within human CD8 memory T-cell populations. We find T-bet and Eomes are broadly expressed in human memory CD8 T cells, with increasing levels of T-bet and Eomes strongly correlating with differentiation from central memory to effector memory and effector subpopulations. Interestingly, T-bet levels directly correlate to subcellular localization, with a higher propensity for nuclear expression of T-bet within T-bethi cells and predominately cytoplasmic expression in T-betlo cells. In contrast, Eomes appears to be localized solely to the nucleus. In murine CD8 T cells, T-bet can be nuclear, cytoplasmic, or both; however, Eomes is detectable in both compartments suggesting differential regulation compared to humans. Additionally, in humans, Eomes tightly correlated with nuclear T-bet suggesting T-bet localization might impact Eomes expression. Together, our data provide a novel mechanism for CD8 T-cell differentiation in humans and mice based on subcellular localization of T-bet, and reveal the likely presence of previously unknown regulation mechanisms for these critical lineage defining transcription factors.
18
Wallace, D. J., T. Atsumi, M. Daniels, A. Hammer, P. Meizlik, H. Quasny, A. Schwarting, F. Zhang, and D. Roth. "POS0697 SAFETY OF BELIMUMAB IN ADULT PATIENTS WITH SYSTEMIC LUPUS ERYTHEMATOSUS: A LARGE INTEGRATED SAFETY ANALYSIS OF CONTROLLED CLINICAL TRIAL DATA." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 596.2–597. http://dx.doi.org/10.1136/annrheumdis-2021-eular.2373.
Full textAbstract:
Background:Belimumab (BEL), a monoclonal antibody that antagonizes B-lymphocyte stimulator, was first approved in 2011 for active, autoantibody-positive systemic lupus erythematosus (SLE). BEL has been studied for over 10 years; and while safety data from individual trials have been informative, a large integrated safety analysis has not yet been conducted.Objectives:Perform pooled analyses to evaluate the safety of BEL in adult patients with SLE.Methods:Aggregate analyses were performed using safety data for patients ≥18 years of age pooled from six randomised, placebo (PBO)-controlled BEL clinical trials (GSK studies: LBSL02, 110752, 110751, 112341, 113750, and 115471). Patients from GSK studies LBSL02, 110752, and 110751 received intravenous (IV) BEL 1, 4 (LBSL02 only), or 10 mg/kg, or PBO on Days 1, 14, 28, and every 28 days thereafter. Patients from GSK studies 113750 and 115471 received IV BEL 10 mg/kg or PBO on Days 1, 14, 28, and every 28 days thereafter. Patients from GSK study 112341 received subcutaneous (SC) BEL 200 mg, or PBO weekly. Safety analyses included the incidence of adverse events (AEs), serious AEs (SAEs), severe AEs, AEs of special interest (AESI), and mortality of BEL (all doses and formulations combined) vs PBO at Week 52.Results:The pooled analysis included 4170 patients. Overall, 81.0% (n=2280/2815) of patients receiving BEL and 76.6% (n=1038/1355) of patients receiving PBO completed their respectively enrolled study; the most common reason for withdrawal was occurrence of an AE in both groups. The majority of patients were female (BEL: 94.5%; PBO: 93.6%), the mean age in both groups was 38 years, and baseline characteristics (race, SLE duration, disease activity, SLE damage, complement levels, anti-dsDNA binding, SLE medication usage) were similar between treatments.The incidence of patients experiencing ≥1 AE, ≥1 SAE, and mortality was similar across treatments (Table 1); the most commonly reported SAEs in both groups were infections and infestations (BEL: 5.4% [n=151/2815]; PBO: 5.9% [n=80/1355]). The mean duration of treatment exposure was similar between groups (BEL: 334.1 days; PBO: 325.3 days).A greater proportion of patients experienced AESI with BEL vs PBO for post-infusion/injection systemic reactions (from IV or SC administration) and depression/suicide/self-injury (Table 1). The proportion of patients experiencing an AESI of infections and malignancies was similar between groups.Conclusion:Consistent with individual studies, BEL demonstrated a similar safety profile to PBO in this large integrated safety analysis of six trials. These results support a positive benefit–risk profile of BEL in the treatment of adult SLE.Funding:GSKTable 1.Pooled AE dataN (%)PBO (IV + SC)N=1355BEL (IV + SC)N=2815AE1184 (87.4)2440 (86.7)SAE230 (17.0)421 (15.0)Severe AE (severe or life threatening)209 (15.4)377 (13.4)AE resulting in study drug discontinuation109 (8.0)184 (6.5)Death6 (0.4)16 (0.6)AESIPost-infusion/injection systemic reactions*110 (8.1)286 (10.2)Serious2 (0.1)13 (0.5)All infections of special interest (OIs, HZ, TB, sepsis)97 (7.2)173 (6.1)Serious17 (1.3)40 (1.4)All OIs92 (6.8)157 (5.6)Active TB5 (0.4)4 (0.1)All HZ59 (4.4)106 (3.8)All sepsis10 (0.7)20 (0.7)Malignancies excluding NMSC2 (0.1)8 (0.3)Including NMSC3 (0.2)12 (0.4)Depression (inc. mood disorders and anxiety)/suicide/self-injury92 (6.8)210 (7.5)Serious5 (0.4)9 (0.3)*Occurring on or within 3 days of infusion/injection date.HZ, herpes zoster; NMSC, non-melanoma skin cancer; OIs, opportunistic infections; TB, tuberculosisAcknowledgements:Medical writing assistance was provided by Helen Taylor, Fishawack Indicia Ltd., UK, part of Fishawack Health, and was funded by GSK.Disclosure of Interests:Daniel J. Wallace Speakers bureau: GSK, Consultant of: GSK, Tatsuya Atsumi Speakers bureau: GSK, Consultant of: GSK, Grant/research support from: GSK, Mark Daniels Shareholder of: GSK, Employee of: GSK, Anne Hammer Shareholder of: GSK, Employee of: GSK, Paige Meizlik Shareholder of: GSK, Employee of: GSK, Holly Quasny Shareholder of: GSK, Employee of: GSK, Andreas Schwarting Speakers bureau: Novartis, Roche, GSK, Pfizer, Amgen, Consultant of: GSK, Grant/research support from: AbbVie, Pfizer, Novartis, GSK, Actelion, Fengchun Zhang: None declared, David Roth Shareholder of: GSK, Employee of: GSK
19
Lu, Jinghua, Kristopher Marjon, Lorraine Marnell, Carolyn Mold, Terry Du Clos, and Peter Sun. "The Structure and Function of Acute Phase Proteins: C-Reactive Protein and Serum Amyloid A in Innate Immunity (110.21)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 110.21. http://dx.doi.org/10.4049/jimmunol.186.supp.110.21.
Full textAbstract:
Abstract During an acute infection, serum levels of certain proteins will be increased dramatically at the early stage of the infection, which are so-called acute phase proteins (APPs). Among them, C-reactive protein (CRP) and Serum Amyloid A (SAA) are two major APPs in humans and therefore they have long been used as clinical biomarkers to monitor the inflammation and the outcome of therapy. However, the physiological function of CRP and SAA remains to be better characterized. In our study, we have shown that CRP can functionally activate Fc receptors pathways, particularly FcγRs and FcαRI (CD89), resulting in the phagocytosis of microbial pathogens and cytokine secretion, such as IL6, and IL8. The ability of CRP to activate FcγRs and FcαRI defines a novel function for acute phase proteins in inflammatory responses involving neutrophils and macrophages and also highlights the innate aspect of otherwise humoral immunity-associated antibody receptors. Furthermore, SAA was shown to be able to bind Gram-positive bacteria. We have now determined the X-ray structure of SAA at 2.7Å resolution. The natural hexameric SAA structure revealed a dimeric architecture arranged as two trimers. We also discovered that SAA hexamer could undergo a transition to monomers that are able to bind and activate Toll-like receptor 2 and 4. Taken together, our studies highlighted CRP and SAA as the powerful first lines of host immune defense during acute infection.
20
Plumlee, Courtney, Joshua Obar, and Leo Lefrançois. "Defining the early effector CD8 T cell population: plastic cells capable of populating the short-lived and memory pools. (110.11)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 110.11. http://dx.doi.org/10.4049/jimmunol.188.supp.110.11.
Full textAbstract:
Abstract Naïve antigen specific CD8 T cells expand in response to infection and can be phenotypically separated into distinct effector populations at the peak of the response, which include memory precursor effector cells (MPEC) and short-lived effector cells (SLEC). Shortly after infection, a third population called early effector cells (EEC) predominate in the antigen specific response and give rise to both the MPEC and SLEC populations. To understand if EEC populations were pre-committed to either an MPEC or SLEC fate, we purified EEC from mice infected with Listeria monocytogenes (LM) or vesicular stomatitis virus (VSV), in which the ratio of EEC/SLEC/MPEC at the peak of the response is known to be different. Transfers of sorted EEC into uninfected hosts revealed that EEC were pre-programmed to differentiate based on early signals received from the different infection settings. Additionally, gene expression analysis revealed that a subset of genes was differentially regulated between EEC derived from VSV or LM infections. Surprisingly, when these same EEC were transferred early into mismatched infected hosts, the transferred EEC were diverted from their original commitment programming. These results delineate a model of differentiation where EEC are programmed to form MPEC or SLEC, but where additional inflammatory signals can alter this program. Understanding the molecular regulation of the development of an EEC to a memory cell will facilitate rational vaccine design.
21
Henrickson, Sarah, Balimkiz Senman, Michael Quigley, Gabriela Alexe, Susanne Stutte, Jonathan Jesneck, Matteo Iannacone, et al. "Antigen availability is a critical determinant of in vivo CD8+ T cell-dendritic cell interaction kinetics and initiates effector/memory fate decisions (110.21)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 110.21. http://dx.doi.org/10.4049/jimmunol.188.supp.110.21.
Full textAbstract:
Abstract Naïve CD8+ T cells are activated through interactions with antigen (Ag) bearing dendritic cells (DCs) in lymph nodes (LNs). Multiphoton intravital microscopy (MP-IVM) of LNs has demonstrated that T cell activation occurs in three phases. The duration of the initial phase of transient, serial DC-T cell interactions is inversely related to Ag dose. It had been assumed that the second phase, characterized by stable DC-T cell contacts, is necessary for T cell activation, however, here we show that this is not always the case. T cells interacting with DCs presenting Ag at low abundance and with a short half-life did not transition from phase one to phase two, whereas a higher dose of the same Ag yielded robust phase two transition. T cells exposed to either antigenic constellation proliferated and developed equivalent effector functions, including cytokine production and cytotoxicity, over the first two days after priming. There are profound differences in the transcriptome at 12h and 24h after activation between CD8 T cells exposed to antigenic constellations that did or did not promote phase two interactions. Only T cells that had undergone stable contacts gave rise to memory, whereas activating conditions that did not support stable contacts yielded immunological amnesia. T cells can make fate decisions in vivo within a few hours after Ag exposure that result in long-term memory or abortive effector responses and correlate with the kinetics of T cell-DCs interactions.
22
Pisko, Edward J. "Arthritis and allied conditions. Tenth edition. Daniel J. McCarty (editor). Philadelphia, Lea & Febiger, 1985. 1,773 pages. Illustrated. Indexed. $110.00." Arthritis & Rheumatism 29, no. 3 (March 1986): 455. http://dx.doi.org/10.1002/art.1780290335.
Full text
23
Garaiman, A., K. Steigmiller, C. Gebhard, C. Mihai, R. Dobrota, M. Matucci-Cerinic, J. Henes, et al. "POS0877 THE EFFECT OF PLATELET INHIBITORS ON DIGITAL ULCERS IN SYSTEMIC SCLEROSIS - A DERIVATION AND VALIDATION EUSTAR STUDY." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 694.2–695. http://dx.doi.org/10.1136/annrheumdis-2021-eular.3272.
Full textAbstract:
Background:Digital ulcers (DUs) affect half of the patients with systemic sclerosis (SSc) and can be complicated by gangrene and amputation. The direct involvement of platelets in the development of DUs has been suggested by in vitro studies, which encouraged physicians to consider platelet inhibitors as a therapeutic option in the management of DUs. However, until now, there is no clinical study to assess the efficacy of platelet inhibitors for DUs in SSc patients.Objectives:To demonstrate a possible relationship between treatment with platelet inhibitors and the occurrence of DUs at the next follow-up visit in patients with SSc.Methods:This study used prospectively collected data from the European Scleroderma Trials and Research group (EUSTAR) registry. Patients fulfilling the 2013 ACR/EULAR SSc classification criteria with complete longitudinal data on the presence of DUs and platelet inhibitors were included in the analysis. Multiple imputation using a random forest algorithm was implemented to handle missing values.The dataset was split into a derivation and validation cohort. To investigate the response for the binary dependent variable of DUs, a generalized linear mixed model (GLMM) was developed in the derivation cohort and validated using ROC analysis and Brier scores to address discrimination and calibration, respectively.Results:Of 3,463 patients (2,961 in the derivation cohort, 722 in the validation cohort), 453 had current DUs at the baseline and 245 were exposed to platelet inhibitors (table 1).Our GLMM revealed that the exposure to platelet inhibitors is associated with a reduced risk of DUs at the next follow up visit (OR = 0.33, 95% CI = [0.13 to 0.82]). Further factors associated with absence or presence of DUs at the next follow-up visit are shown in figure 1. This confirmed the previously identified risk factors for the presence of DUs, supporting the overall robustness and the validity of our model.The performance was evaluated by ROC curve analysis and showed an AUC = 97.97% (95% CI = [96.93% to 97.67%]) for the derivation cohort and AUC = 77.3% (95% CI = [74.01% to 81.39%]) for the validation cohort, respectively, showing an acceptable discrimination. The Brier score was 0.05 in the derivation cohort and 0.07 in the validation cohort, suggesting a good calibration of the model.Conclusion:Our model, with acceptable discrimination and good calibration, suggests a positive treatment effect of platelet inhibitors on DUs in clinical practice.Table 1.Baseline characteristics of patients before imputationCharacteristicsOverallDerivation setValidation setn3,4632,691772Age (median [IQR])56.00 [47.00, 66.00]56.00 [47.00, 65.00] 57.00 [48.00, 67.00]Disease duration (median [IQR]) 9.00 [4.00, 16.00] 9.00 [4.00, 16.00] 8.00 [4.00, 15.00]Disease subset = Limited cutaneous SSc (%) 1562 (65.2) 1164 (64.6) 398 (66.9)DUs (%): Current 453 (13.1) 378 (14.0) 75 (9.7)DUs (%): Never 1783 (51.5) 1326 (49.3) 457 (59.2)DUs (%): Previously 1227 (35.4) 987 (36.7) 240 (31.1)mRSS (median [IQR]) 5.00 [2.00, 11.00] 6.00 [2.00, 12.00] 4.00 [1.00, 11.00]Joint Contractures = Yes (%) 881 (26.8) 770 (29.4) 111 (16.5)LVEF (median [IQR])62.00 [60.00, 65.00]60.00 [60.00, 65.00] 65.00 [60.00, 67.00]Dyspnea NYHA III and IV (%)300 (9.5)214 (8.6)86 (12.7)Pulmonary hypertension = Yes (%) 244 (10.7) 200 (11.3) 44 (8.4)Lung fibrosis on HRCT = Yes (%) 685 (46.6) 600 (47.7) 85 (39.7)FVC % predicted (median [IQR])97.00 [82.00, 111.00]95.00 [81.00, 110.00]101.00 [85.00, 115.00]Serum creatinine mg/dl (median [IQR]) 0.70 [0.60, 0.90] 0.70 [0.60, 0.90] 0.70 [0.70, 0.90]Anti-Scl-70 positive = Yes (%) 1147 (33.1) 958 (35.6) 189 (24.5)CRP elevation = Yes (%) 639 (21.1) 490 (20.8) 149 (22.1)Platelet inhibitors therapy = Yes (%) 245 (7.1) 206 (7.7) 39 (5.1)Oral anti-coagulants therapy = Yes (%) 53 (1.5) 50 (1.9) 3 (0.4)Disclosure of Interests:None declared
24
Ghonim, Mohamed A., Amarjit S. Naura, Paulo Rodriguez, Amir Al Khami, Claudia Hernandez, Moselhy S. Mansy, Augusto Ochoa, and Hamid Boulares. "Olaparib, a PARP inhibitor approved for human testing, prevents allergen‐induced airway inflammation and hyperresponsiveness in a mouse model of asthma and reduces proliferation of human CD3/C28‐stimulated CD4+ T cells." FASEB Journal 27, S1 (April 2013). http://dx.doi.org/10.1096/fasebj.27.1_supplement.1107.1.
Full text