scholarly journals Species heterogeneity in macrophage expression of the CD4 antigen.

1987 ◽  
Vol 166 (2) ◽  
pp. 613-618 ◽  
Author(s):  
P R Crocker ◽  
W A Jefferies ◽  
S J Clark ◽  
L P Chung ◽  
S Gordon
Keyword(s):  
T Cells ◽  
Northern Blot ◽  
Mammalian Species ◽  
Blot Hybridization ◽  
Antigen Expression ◽  
Northern Blot Hybridization ◽  
Facs Analysis ◽  
Aids Virus ◽  
Immunoperoxidase Labeling ◽  
Striking Contrast

The CD4 antigen is expressed on T cells of all mammalian species examined and appears to play an important role in the response of T cells to antigen. In humans, the molecule acts as a receptor for the AIDS virus. Previous studies have demonstrated that M phi in the rat and human also express the CD4 antigen, which is indistinguishable from that on T cells. In this paper we demonstrate by FACS analysis, Northern blot hybridization, and immunoperoxidase labeling that, in striking contrast to the rat and human, mouse M phi do not express the CD4 (L3T4) antigen. This species heterogeneity indicates that T cells and M phi regulate CD4 antigen expression independently and that CD4 may not be essential for M phi function.

scholarly journals Induction of hepatic metallothioneins determined at isoprotein and messenger RNA levels in glucocorticoid-treated rats

1988 ◽  
Vol 249 (2) ◽  
pp. 429-433 ◽  
Author(s):  
L D Lehman-McKeeman ◽  
G K Andrews ◽  
C D Klaassen
Keyword(s):  
Detection Limit ◽  
Northern Blot ◽  
Blot Analysis ◽  
Messenger Rna ◽  
Time Course ◽  
Northern Blot Analysis ◽  
Blot Hybridization ◽  
Northern Blot Hybridization ◽  
Single Dosage ◽  
Rna Levels

Induction of metallothionein-I (MT-I) and metallothionein-II (MT-II) by glucocorticoids was determined by h.p.l.c. analysis of proteins and Northern-blot analysis of MT mRNAs. Rats were injected with dexamethasone (0.03-10 mumol/kg) and hepatic concentrations of MTs were determined 24 h later. In control rats, only MT-II was detected (9.4 +/- 2.5 micrograms/g of liver), whereas the hepatic concentration of MT-I was below the detection limit (5 micrograms of MT/g). Dexamethasone did not increase MT-I above the detection limit at any dosage tested, but MT-II increased to 2.5 times control values at dosages of 0.30 mumol/kg and higher. Time-course experiments indicated that MT-II reached a maximum at 24 h after a single dosage of dexamethasone and returned to control values by 48 h. To determine whether dexamethasone increased MT-I in liver, samples were saturated with 109Cd, after which the amount of 109Cd in MT-I and MT-II was determined. Results indicated that, by this approach, MT-I and MT-II could be detected in control rats, and there was approx. 1.8 times more 109Cd in MT-II than in MT-I. At 24 h after administration of dexamethasone (1 mumol/kg), there was a small increase in the amount of 109Cd bound to MT-I, whereas the amount of 109Cd bound to MT-II increased to more than 2 times control values. Northern-blot hybridization with mouse cRNA probes indicated that MT-I and MT-II mRNAs increased co-ordinately after administration of dexamethasone. Thus, although glucocorticoids increase both MT-I and MT-II mRNAs, MT-II preferentially accumulates after administration of dexamethasone.

Comparison of human and porcine group C rotaviruses by Northern blot hybridization analysis

1991 ◽  
Vol 118 (3-4) ◽  
pp. 269-277 ◽  
Author(s):  
Y. Qian ◽  
L. J. Saif ◽  
A. Z. Kapikian ◽  
S. Y. Kang ◽  
B. Jiang ◽  
...  
Keyword(s):  
Northern Blot ◽  
Blot Hybridization ◽  
Hybridization Analysis ◽  
Northern Blot Hybridization

scholarly journals Endothelial cells augment T cell interleukin 2 production by a contact-dependent mechanism involving CD2/LFA-3 interaction.

1990 ◽  
Vol 171 (5) ◽  
pp. 1453-1467 ◽  
Author(s):  
C C Hughes ◽  
C O Savage ◽  
J S Pober
Keyword(s):  
T Cells ◽  
Endothelial Cells ◽  
T Cell ◽  
Mhc Class Ii ◽  
Blot Hybridization ◽  
Interleukin 2 ◽  
Class Ii ◽  
Cell Contact ◽  
Northern Blot Hybridization ◽  
Ifn Gamma

We have demonstrated that endothelial cells (EC) augment IL-2 production by PHA-stimulated PBMC or purified CD4+ T cells and that the increase is apparent both in the amount of soluble IL-2 secreted and in the level of specific mRNA detectable by Northern blot hybridization. The ability of EC to affect levels of IL-2 cannot be reproduced by soluble factors, including the cytokines IL-1, IL-6, IFN-gamma, or TNF, conditioned medium from resting EC or IL-1, IFN-gamma- or TNF-treated EC, or from resting PBMC + EC cultures. Separation of the EC and PBMC by a Transwell membrane demonstrated that cell contact was required for augmentation of IL-2 synthesis and that this effect was unlikely to be mediated by a short-lived soluble signal. The cell-cell interaction required the ligand pair CD2/LFA-3, since augmentation could be inhibited by antibodies to these structures. Antibodies to ICAM-1, LFA-1, CD4, and MHC class II were without effect. A contact-dependent pathway involving CD2/LFA-3 interactions also may be used by EC to augment IL-2 production from T cells stimulated more specifically through the TCR/CD3 complex with antibody OKT3. This pathway provides a proliferative advantage to T cells stimulated with OKT3 in the presence of EC and may also be involved in the proliferative response of resting T cells to allogeneic class II MHC-expressing EC. We propose that EC augmentation of T cell IL-2 synthesis may be critical in the ability of EC to elicit primary T cell antigen responses and may have consequences for the development of localized cell-mediated immune reactions.

Sign in / Sign up

Export Citation Format

Share Document