PMID- 9445015
OWN - NLM
STAT- MEDLINE
DCOM- 19980218
LR  - 20240409
IS  - 0022-538X (Print)
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Linking)
VI  - 72
IP  - 2
DP  - 1998 Feb
TI  - Activation of antiviral protein kinase leads to immunoglobulin E class switching 
      in human B cells.
PG  - 1171-6
AB  - An epidemiologic association between viral infections and the onset of asthma and 
      allergy has been documented. Also, evidence from animal and human studies has 
      suggested an increase in antigen-specific immunoglobulin E (IgE) production 
      during viral infections, and elevated levels of IgE are characteristic of human 
      asthma and allergy. Here, we provide molecular evidence for the roles of viral 
      infection and of activation of the antiviral protein kinase (PKR) 
      (double-stranded-RNA [dsRNA]-activated protein kinase) in the induction of IgE 
      class switching. The presence of dsRNA, a known component of viral infection and 
      an activator of PKR, induced IgE class switching as detected by the expression of 
      germ line epsilon in the human Ramos B-cell line. Furthermore, dsRNA treatment of 
      Ramos cells resulted in the activation of PKR and in vivo activation of the 
      NF-kappaB complex. Interestingly, infection of Ramos cells with rhinovirus 
      (common cold virus) serotypes 14 and 16 resulted in the induction of germ line 
      epsilon expression. To further evaluate the role of PKR in the viral induction of 
      IgE class switching, we infected Ramos cells with two different vaccinia virus 
      (cowpox virus) strains. Infection with wild-type vaccinia virus failed to induce 
      germ line epsilon expression; however, a deletion mutant of vaccinia virus 
      (VP1080) lacking the PKR-inhibitory polypeptide E3L induced the expression of 
      germ line epsilon. Collectively, the results of our study define a common 
      molecular mechanism underlying the role of viral infections in IgE class 
      switching and subsequent induction of IgE-mediated disorders such as allergy and 
      asthma.
FAU - Rager, K J
AU  - Rager KJ
AD  - Asthma and Allergy Center, Department of Medicine, The Johns Hopkins University 
      School of Medicine, Baltimore, Maryland 21224-6821, USA.
FAU - Langland, J O
AU  - Langland JO
FAU - Jacobs, B L
AU  - Jacobs BL
FAU - Proud, D
AU  - Proud D
FAU - Marsh, D G
AU  - Marsh DG
FAU - Imani, F
AU  - Imani F
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Virol
JT  - Journal of virology
JID - 0113724
RN  - 37341-29-0 (Immunoglobulin E)
RN  - EC 2.7.11.1 (eIF-2 Kinase)
SB  - IM
MH  - B-Lymphocytes/*immunology/*virology
MH  - Gene Expression Regulation, Viral
MH  - Humans
MH  - Immunoglobulin Class Switching/drug effects/*genetics
MH  - Immunoglobulin E/*genetics/immunology
MH  - Mutation
MH  - Tumor Cells, Cultured
MH  - Vaccinia/genetics/*immunology
MH  - *Vaccinia virus
MH  - eIF-2 Kinase/*genetics/immunology/pharmacology
PMC - PMC124593
EDAT- 1998/01/28 00:00
MHDA- 1998/01/28 00:01
PMCR- 1998/02/01
CRDT- 1998/01/28 00:00
PHST- 1998/01/28 00:00 [pubmed]
PHST- 1998/01/28 00:01 [medline]
PHST- 1998/01/28 00:00 [entrez]
PHST- 1998/02/01 00:00 [pmc-release]
AID - 1267 [pii]
AID - 10.1128/JVI.72.2.1171-1176.1998 [doi]
PST - ppublish
SO  - J Virol. 1998 Feb;72(2):1171-6. doi: 10.1128/JVI.72.2.1171-1176.1998.