PMID- 9767423
OWN - NLM
STAT- MEDLINE
DCOM- 19981019
LR  - 20190512
IS  - 0019-2805 (Print)
IS  - 1365-2567 (Electronic)
IS  - 0019-2805 (Linking)
VI  - 94
IP  - 3
DP  - 1998 Jul
TI  - Lymphotoxin-alpha is an important autocrine factor for CD40 + 
      interleukin-4-mediated B-cell activation in normal and atopic donors.
PG  - 395-402
AB  - Stimulation of human B cells with anti-CD40 + interleukin-4 (IL-4) results not 
      only in proliferation and immunoglobulin E (IgE)-production, but also increased 
      production of the cytokine lymphotoxin-alpha (LT-alpha) (formerly also known as 
      tumour necrosis factor-beta (TNF-beta)). Here, we studied the role of LT-alpha 
      (TNF-beta) in B cells following stimulation with anti-CD40 + IL-4 from normal 
      versus atopic donors. Anti-CD40 + IL-4 stimulation of peripheral blood 
      mononuclear cells (PBMC) from atopic donors resulted in enhanced production of 
      soluble LT-alpha (TNF-beta) and increased membrane LT-alpha (TNF-beta) expression 
      on the B cells compared with normal donors. Functional evaluation of LT-alpha 
      (TNF-beta) in CD40 + IL-4-stimulated B cells shows that recombinant LT-alpha 
      (TNF-beta) induces proliferation of B cells and enhances CD40 + IL-4-mediated 
      B-cell proliferation and IgE synthesis in both normal and atopic donors in a 
      dose-dependent manner. These findings were supported by semiquantitative analysis 
      of epsilon-germline transcripts using reverse transcription-polymerase chain 
      reaction (RT-PCR) showing increased epsilon-germline transcription in the 
      presence of LT-alpha. Furthermore, addition of anti-LT-alpha (anti-TNF-beta) to 
      CD40 + IL-4-stimulated B cells partially inhibited proliferation and IgE 
      synthesis in a dose-dependent manner indicating a role of endogenous LT-alpha 
      (TNF-beta) production by B cells during continued CD40 + IL-4 stimulation. These 
      data suggest that LT-alpha (TNF-beta) plays a potentially significant role during 
      B-cell proliferation and IgE synthesis. Moreover, LT-alpha (TNF-beta) production 
      seems to be differentially regulated in B cells from normal and atopic donors.
FAU - Worm, M
AU  - Worm M
AD  - Department of Dermatology, Charite-Virchow Klinikum, Humboldt Universitat, 
      Berlin, Germany.
FAU - Ebermayer, K
AU  - Ebermayer K
FAU - Henz, B
AU  - Henz B
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Immunology
JT  - Immunology
JID - 0374672
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (CD40 Antigens)
RN  - 0 (Immunoglobulin epsilon-Chains)
RN  - 0 (Lymphotoxin-alpha)
RN  - 0 (Recombinant Proteins)
RN  - 207137-56-2 (Interleukin-4)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Antibodies, Monoclonal/*pharmacology
MH  - B-Lymphocytes/drug effects/*immunology
MH  - CD40 Antigens/*immunology
MH  - Cell Membrane/immunology
MH  - Cells, Cultured
MH  - Dose-Response Relationship, Immunologic
MH  - Humans
MH  - Hypersensitivity/*immunology
MH  - Immunoglobulin E/biosynthesis
MH  - Immunoglobulin epsilon-Chains/genetics
MH  - Immunohistochemistry
MH  - Interleukin-4/*pharmacology
MH  - Lymphocyte Activation/drug effects
MH  - Lymphotoxin-alpha/biosynthesis/pharmacology/*physiology
MH  - Polymerase Chain Reaction
MH  - Recombinant Proteins/pharmacology
MH  - Transcription, Genetic
PMC - PMC1364259
EDAT- 1998/10/10 00:00
MHDA- 1998/10/10 00:01
PMCR- 1999/07/01
CRDT- 1998/10/10 00:00
PHST- 1998/10/10 00:00 [pubmed]
PHST- 1998/10/10 00:01 [medline]
PHST- 1998/10/10 00:00 [entrez]
PHST- 1999/07/01 00:00 [pmc-release]
AID - 10.1046/j.1365-2567.1998.00520.x [doi]
PST - ppublish
SO  - Immunology. 1998 Jul;94(3):395-402. doi: 10.1046/j.1365-2567.1998.00520.x.