Human immune responses are heterogeneous and may involve antagonism between T helper (TH) lymphocyte subsets and their cytokines. Atopy is characterized by immediate immunoglobulin E (IgE)-mediated hypersensitivity to agents such as dust mites and pollen, and it underlies the increasingly prevalent disorder asthma. Among Japanese schoolchildren, there was a strong inverse association between delayed hypersensitivity to Mycobacterium tuberculosis and atopy. Positive tuberculin responses predicted a lower incidence of asthma, lower serum IgE levels, and cytokine profiles biased toward TH1 type. Exposure and response to M. tuberculosis may, by modification of immune profiles, inhibit atopic disorder.
7P % Control dbcAMP apoptosir (O2mM) 6hr 2.W.6 0.9iO.1 20hr 61.W.5 28.9i3.8' ResultsTPI mRNA was detected in both controls and treated cells. However, densilometric analysis revealed that TPI mRNA levels in treated cells (mean f SEM = 5 . M . 1 arbiirary unils) was more than two-fold afler 6 hours in culture for 5mM and IOmM sodium butyrate compared to controls (2.OM.1 arbiirary unls). There was no significant difference in levels of TPI mRNA between controls and cells treated with 1mM sodium butyrate (2.M.1 arbiirary unils) at all time points. Conclusions This study demonstrates an upregulation of TPI gene expression (a so-called housekeeping gene) by an experimental stimulus, and provides insight into the potential therapeutic beneffi of treatment of the neurological disorders associated with TPI deficiency."he 12 subtypes d IFNa are related q t d c i n e s with antiviral antiprdiferative and i m m u n a n c d u l a t a y activities. All d the subtypes are believed to have similar functions h t suMe differences can be seen, fcr example in the antiviral activities d the different subtypes To investigate further differences, 8 HPLC purified IFNa s u -were tested for activity on human B mils All d the subtypes, in mstimulation with anti-IgM, caused an increase in B cell prdiferation at high anaentrations (lOOOU/ml), with the stception d IFNal. H w e v e r , IFNa8 had mu& greater activity than t h e other subtypes, increasing p d i f e r a t i m at 58100 f d d Iwa amcentrations than the other s u -. H w e v e r , bdh l F N d and IFNa8 were able to increase B cell surface expression d MHC class I with similar dose respcnses and magnitudes. These results indicate the prtzsence d at least 2 IFNa signalling pathways in B cells, me d which causes MHC I induction and i s activated to the Same extent by all type I IFNs and another which induoes B cell p d i f e r a t i m and i s preferentially activated b>l IFNa8.To eluadate these pathways, we are investigating the transcription factors activated in B cells i n r e s p s e to the IFNa subtypes. Neutrophil apoptosis is an important mechanism underlying the removal of redundant, but potentially tissuedamaging neutrophils ffom an inflamed site.The ability of many pro-inflammatory agents to impede neutrophil apoptosis suggests that such mediators act both to enhance cell activation and increase neutrophil longevity. Inhibition of neutrophil apoptosis is also observed in response to mediators that elevate CAMP levels (Rossi et al.. Biochem Biophys Res Commun, 1995; 217:892-9). an effect which may counteract their otherwise useful anti-inflammatory properties. In view of reports that NO donors can induce apoptosis in other myeloid cells we have examined the potential for these agents to Serve a dual function of both inhibiting cell activation and promoting apoptosis. Human neutrophils were isolated &om peripheral blood using plasma-Percoll gradients and cultured for 6 and 20 hrs in the presence of the NO donors GEA3162, SIN-I and SNAP and the cell permeable cyclic nucleotide ...
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.