PMID- 15578334
OWN - NLM
STAT- MEDLINE
DCOM- 20050421
LR  - 20061115
IS  - 0947-7349 (Print)
IS  - 0947-7349 (Linking)
VI  - 112
IP  - 10
DP  - 2004 Nov
TI  - Expression of gonadotropin-releasing hormone type-I (GnRH-I) and type-II 
      (GnRH-II) in human peripheral blood mononuclear cells (PMBCs) and regulation of 
      B-lymphoblastoid cell proliferation by GnRH-I and GnRH-II.
PG  - 587-94
AB  - GnRH-I and its receptor (GnRHR-I) have previously been demonstrated and shown to 
      be biologically active in the immune system, notably within T cells. Recently 
      however a second form of GnRH (GnRH-II) has been described in the human. The 
      function of both these neuropeptides in B lymphocytes has not previously been 
      explored. The present study investigates GnRH-I and GnRH-II expression in human 
      peripheral mononuclear blood cells (PMBCs) and B lymphoblastoid cells (B-LCLs), 
      as well as their action in regulating B-LCL proliferation in the presence and 
      absence of interleukin-2 (IL-2), both in GnRHR-I mutated lymphocytes and in a 
      normal control. RT-PCR and immunocytochemistry identified locally produced GnRH-I 
      and GnRH-II in all cell groups. Treatment of normal B-LCLs with GnRH-I (10 (-9) M 
      and 10 (-5) M) or with interleukin-2 (IL-2) (50 IU/ml) resulted in a significant 
      increase in cell proliferation compared with the untreated control. IL-2 and 
      GnRH-I (10 (-7) M, 10 (-6) M, 10 (-5) M) induced greater proliferation in normal 
      B-LCLs than IL-2 treatment alone. No significant proliferation occurred in 
      GnRHR-I defective B-LCLs, in response to either GnRH-I (10 (-9) and 10 (-5) M) or 
      IL-2 treatment, nor to IL-2 and GnRH-I (10 (-10) to 10 (-5) M) co-treatment when 
      compared to controls. Co-incubation of IL-2 and IL-2 + GnRH 10 (-5) M with a GnRH 
      antagonist (Cetrorelix; 10 (-6) M) significantly attenuated the proliferation in 
      normal B-LCLs. GnRH-II did not affect proliferation of normal B-LCLs alone, and 
      did not alter the proliferative response to IL-2. Further investigation is 
      required to clarify the physiological relevance of local GnRH-I/GnRH-II in immune 
      system responsiveness.
FAU - Tanriverdi, F
AU  - Tanriverdi F
AD  - Department of Endocrinology, Erciyes University Medical School, Talasyolu, 
      Kayseri, Turkey. fatihtan@erciyes.edu.tr
FAU - Gonzalez-Martinez, D
AU  - Gonzalez-Martinez D
FAU - Silveira, L F G
AU  - Silveira LF
FAU - Hu, Y
AU  - Hu Y
FAU - Maccoll, G S
AU  - Maccoll GS
FAU - Travers, P
AU  - Travers P
FAU - Bouloux, P M G
AU  - Bouloux PM
LA  - eng
PT  - Journal Article
PL  - Germany
TA  - Exp Clin Endocrinol Diabetes
JT  - Experimental and clinical endocrinology & diabetes : official journal, German 
      Society of Endocrinology [and] German Diabetes Association
JID - 9505926
RN  - 0 (Interleukin-2)
RN  - 33515-09-2 (Gonadotropin-Releasing Hormone)
RN  - 91097-16-4 (LHRH, His(5)-Trp(7)-Tyr(8)-)
SB  - IM
MH  - Adult
MH  - B-Lymphocytes/drug effects/immunology/*physiology
MH  - Cell Division/drug effects
MH  - Gonadotropin-Releasing Hormone/*analogs & derivatives/*genetics/pharmacology
MH  - Humans
MH  - Interleukin-2/pharmacology
MH  - Leukocytes, Mononuclear/*physiology
MH  - Lymphocyte Activation/drug effects
MH  - Reference Values
MH  - Reverse Transcriptase Polymerase Chain Reaction
EDAT- 2004/12/04 09:00
MHDA- 2005/04/22 09:00
CRDT- 2004/12/04 09:00
PHST- 2004/12/04 09:00 [pubmed]
PHST- 2005/04/22 09:00 [medline]
PHST- 2004/12/04 09:00 [entrez]
AID - 10.1055/s-2004-830404 [doi]
PST - ppublish
SO  - Exp Clin Endocrinol Diabetes. 2004 Nov;112(10):587-94. doi: 
      10.1055/s-2004-830404.