PMID- 1677813
OWN - NLM
STAT- MEDLINE
DCOM- 19910906
LR  - 20190609
IS  - 0006-3002 (Print)
IS  - 0006-3002 (Linking)
VI  - 1093
IP  - 2-3
DP  - 1991 Jul 10
TI  - CD3-dependent increase in cyclic AMP in human T-cells following stimulation of 
      the CD2 receptor.
PG  - 178-83
AB  - We have previously shown that stimulation of the Ti/CD3 receptor complex on human 
      T-cells potentiates adenylate cyclase activation by adenosine or forskolin. 
      Anti-CD2 receptor antibodies shared with anti-CD3 antibodies the ability to 
      potentiate dose dependently the adenosine- and forskolin-stimulated cyclic 
      adenosine monophosphate (cAMP) accumulation, whereas stimulation of the CD45 
      receptor had no effect on cyclase activity. Modulation of the CD3 complex with 
      anti-CD3 antibodies was found to decrease the CD2 receptor effect on adenylate 
      cyclase activity greatly. The possible involvement of CD3-stimulated 
      phospholipase C (PLC) activation on the cAMP potentiation was examined using 
      HPB-ALL cells that express a CD3 complex with a defect coupling to PLC. 
      Stimulation of the CD3 complex on HPB-ALL cells had only slight effects on 
      adenosine-stimulated cAMP formation, whereas the effect on forskolin-stimulated 
      cAMP was virtually unchanged. The CD3 effect was further analyzed in Jurkat cell 
      membranes. In contrast to the results obtained after stimulation of intact cells, 
      it was found that OKT3 stimulation of membranes did not potentiate the forskolin 
      response. Finally, we tested whether inhibition of endogenous adenylate cyclase 
      agonist production affected the CD3 effect. Inhibition of adenosine production or 
      adenosine breakdown with 8-p-sulphophenyl theophylline (8-PST) or adenosine 
      deaminase (ADA), respectively, did not alter the CD3 effects. Indometacin, which 
      inhibits prostaglandin production, also had no effect. Together, these data show 
      that stimulation of the CD2 receptor potentiates adenylate cyclase responses by a 
      mechanism that is dependent on CD3 expression. Furthermore, the CD3 effect on 
      cAMP appears to be mediated by two different mechanisms, one which is, and one 
      which is not dependent on PLC. Finally, this effect is not due to an endogenous 
      production of adenylate cyclase agonists.
FAU - Kvanta, A
AU  - Kvanta A
AD  - Department of Pharmacology, Karolinska Institutet, Stockholm, Sweden.
FAU - Jondal, M
AU  - Jondal M
FAU - Fredholm, B B
AU  - Fredholm BB
LA  - eng
PT  - Journal Article
PL  - Netherlands
TA  - Biochim Biophys Acta
JT  - Biochimica et biophysica acta
JID - 0217513
RN  - 0 (Antigens, CD)
RN  - 0 (Antigens, Differentiation, T-Lymphocyte)
RN  - 0 (CD2 Antigens)
RN  - 0 (CD3 Complex)
RN  - 0 (Prostaglandin Antagonists)
RN  - 0 (Receptors, Antigen, T-Cell)
RN  - 0 (Receptors, Immunologic)
RN  - 0 (Vasodilator Agents)
RN  - 1F7A44V6OU (Colforsin)
RN  - 35920-39-9 (Adenosine-5'-(N-ethylcarboxamide))
RN  - E0399OZS9N (Cyclic AMP)
RN  - EC 3.1.4.- (Type C Phospholipases)
RN  - EC 4.6.1.1 (Adenylyl Cyclases)
RN  - K72T3FS567 (Adenosine)
SB  - IM
MH  - Adenosine/analogs & derivatives/antagonists & inhibitors/pharmacology
MH  - Adenosine-5'-(N-ethylcarboxamide)
MH  - Adenylyl Cyclases/*metabolism
MH  - Antigens, CD/*metabolism
MH  - Antigens, Differentiation, T-Lymphocyte/*metabolism
MH  - CD2 Antigens
MH  - CD3 Complex
MH  - Cell Line
MH  - Colforsin/pharmacology
MH  - Cyclic AMP/*metabolism
MH  - Humans
MH  - Prostaglandin Antagonists/pharmacology
MH  - Receptors, Antigen, T-Cell/*metabolism
MH  - Receptors, Immunologic/*metabolism
MH  - T-Lymphocytes/drug effects/*metabolism
MH  - Type C Phospholipases/metabolism
MH  - Vasodilator Agents/pharmacology
EDAT- 1991/07/10 00:00
MHDA- 1991/07/10 00:01
CRDT- 1991/07/10 00:00
PHST- 1991/07/10 00:00 [pubmed]
PHST- 1991/07/10 00:01 [medline]
PHST- 1991/07/10 00:00 [entrez]
AID - 0167-4889(91)90120-M [pii]
AID - 10.1016/0167-4889(91)90120-m [doi]
PST - ppublish
SO  - Biochim Biophys Acta. 1991 Jul 10;1093(2-3):178-83. doi: 
      10.1016/0167-4889(91)90120-m.