PMID- 2850959
OWN - NLM
STAT- MEDLINE
DCOM- 19890309
LR  - 20190813
IS  - 0303-7207 (Print)
IS  - 0303-7207 (Linking)
VI  - 60
IP  - 2-3
DP  - 1988 Dec
TI  - Retention of cyclic AMP response to TSH in a cloned human thyrocyte/T cell 
      hybridoma (HY2-15).
PG  - 233-8
AB  - Our observation of a human T cell leukemia cell (Molt 4) demonstrating low 
      affinity thyroid-stimulating hormone (TSH) responses, as evidenced by generation 
      of cyclic AMP, led us to test Molt 4 cells as a suitable partner for 
      immortalizing high affinity TSH receptors present on human thyroid cells. 
      Therefore, we generated a hybridoma (HY2-15) by a fusion between thyroid 
      monolayer cells from a patient with Graves' disease, and a 
      hypoxanthine-aminopterin-thymidine (HAT)-sensitive variant of this human T cell 
      leukemia line, Molt 4-8AGR. The hybrid nature of HY2-15 was confirmed by DNA 
      histograms using propidium iodide and flow cytometry. Karyotyping showed the 
      HY2-15 cells to have five sets of chromosomes and human leukocyte antigen (HLA) 
      class I determination revealed the presence of an additional HLA class I antigen 
      (A2) not present on the Molt 4 partner cells. The established, cloned, hybridoma 
      cells showed a greater than 30-fold increase in cyclic AMP release after 
      stimulation with bovine TSH (bTSH, 1 mU/ml) with a minimum detectable stimulating 
      dose of less than 10 microU/ml bTSH. However, no other thyroid-specific functions 
      could be detected. Furthermore, HY2-15 cells failed to express HLA class II 
      antigens either constitutively or in response to recombinant human gamma 
      interferon (IF) and a variety of other stimuli, data similar to the Molt 4 
      partner cells but in contrast to human thyroid cells which show high sensitivity 
      to gamma IF. The preservation of highly sensitive TSH responsiveness in a 
      proliferating cell offers a unique approach to the study of human TSH receptor 
      function.
FAU - Martin, A
AU  - Martin A
AD  - Department of Medicine, Mount Sinai School of Medicine, New York, NY.
FAU - Platzer, M
AU  - Platzer M
FAU - Davies, T F
AU  - Davies TF
LA  - eng
GR  - DK28242/DK/NIDDK NIH HHS/United States
GR  - DK35764/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Ireland
TA  - Mol Cell Endocrinol
JT  - Molecular and cellular endocrinology
JID - 7500844
RN  - 0 (HLA Antigens)
RN  - 0 (Receptors, Thyrotropin)
RN  - 0 (Recombinant Proteins)
RN  - 82115-62-6 (Interferon-gamma)
RN  - 9002-71-5 (Thyrotropin)
RN  - E0399OZS9N (Cyclic AMP)
SB  - IM
MH  - Cell Division
MH  - Clone Cells
MH  - Cyclic AMP/*biosynthesis
MH  - Dose-Response Relationship, Drug
MH  - Graves Disease
MH  - HLA Antigens/analysis/genetics
MH  - Humans
MH  - Hybridomas/*metabolism
MH  - Interferon-gamma/pharmacology
MH  - Karyotyping
MH  - Leukemia, T-Cell/*metabolism
MH  - Phenotype
MH  - Receptors, Thyrotropin/physiology
MH  - Recombinant Proteins
MH  - Thyrotropin/*pharmacology
MH  - Tumor Cells, Cultured
EDAT- 1988/12/01 00:00
MHDA- 1988/12/01 00:01
CRDT- 1988/12/01 00:00
PHST- 1988/12/01 00:00 [pubmed]
PHST- 1988/12/01 00:01 [medline]
PHST- 1988/12/01 00:00 [entrez]
AID - 10.1016/0303-7207(88)90183-9 [doi]
PST - ppublish
SO  - Mol Cell Endocrinol. 1988 Dec;60(2-3):233-8. doi: 10.1016/0303-7207(88)90183-9.