Role of macrophages in D-penicillamine-induced stimulation of DNA synthesis in lymph node cells

1977 ◽  
pp. 295-302 ◽  
Author(s):  
E. Arrigoni-Martelli ◽  
L. Binderup ◽  
E. Bramm
Keyword(s):  
Lymph Node ◽  
Dna Synthesis ◽  
Lymph Node Cells ◽  
Stimulation Of

Role of plasma membranes in stimulation of RNA-directed DNA synthesis

Nature ◽  
1976 ◽  
Vol 262 (5571) ◽  
pp. 805-807 ◽  
Author(s):  
L. C. PADHY ◽  
S. K. KAR ◽  
K. K. RAO ◽  
M. R. DAS
Keyword(s):  
Dna Synthesis ◽  
Plasma Membranes ◽  
Stimulation Of

scholarly journals Anti-Interleukin-15 Prevents Arthritis in Borrelia-Vaccinated and -Infected Mice

2006 ◽  
Vol 13 (2) ◽  
pp. 289-296 ◽  
Author(s):  
Corey A. Amlong ◽  
Dean T. Nardelli ◽  
Sara Heil Peterson ◽  
Thomas F. Warner ◽  
Steven M. Callister ◽  
...  
Keyword(s):  
Lymph Node ◽  
Significant Role ◽  
Inflammatory Cells ◽  
Interleukin 17 ◽  
Memory Cells ◽  
Present Evidence ◽  
Receptor Alpha ◽  
Lymph Node Cells ◽  
Interleukin 15 ◽  
Stimulation Of

ABSTRACT We showed previously that interleukin-17 (IL-17) plays a significant role in the induction of arthritis associated with Borrelia vaccination and challenge. Little information, however, is available about the chain of immunologic events that leads to the release of IL-17. The production of IL-17 has been linked to stimulation of memory cells by IL-15. Therefore, we hypothesized that IL-15 is involved in the induction of arthritis associated with Borrelia vaccination and infection of mice. Here we present evidence that treatment of Borrelia-vaccinated and -infected mice with anti-IL-15 antibody prevents swelling of the hind paws. More importantly, both anti-IL-15 antibody- and recombinant IL-15 receptor alpha-treated Borrelia-vaccinated and -infected mice were free of major histopathologic indications of arthritis, including hyperplasia, hypertrophy, and vilus formation of the synovium. Similarly, the synovial space and perisynovium were free of inflammatory cells. By contrast, the synovium of nontreated Borrelia-vaccinated and -infected mice had overt hyperplasia, hypertrophy, and vilus formation. Moreover, the synovial space and perisynovium were infiltrated with neutrophils, macrophages, and lymphocytes. Finally, we show that recombinant IL-15 stimulates the release of IL-17 from lymph node cells obtained near the arthritic site. These results suggest that IL-15 plays a major role in orchestrating IL-17 induction of arthritis associated with Borrelia-vaccinated and -infected mice.

Role of polyamines in glucocorticoid effects on pancreatic acinar AR42J cell growth and differentiation

1992 ◽  
Vol 262 (2) ◽  
pp. G285-G290
Author(s):  
C. D. Logsdon ◽  
F. Alves ◽  
S. Rosewicz
Keyword(s):  
Cell Growth ◽  
Dna Synthesis ◽  
Mrna Levels ◽  
Ar42j Cells ◽  
Glucocorticoid Induction ◽  
Cell Growth And Differentiation ◽  
Ar42j Cell ◽  
Inhibition Of Dna Synthesis ◽  
Stimulation Of

We previously found that glucocorticoids inhibit growth and increase differentiation in rat pancreatic acinar AR42J cells. In the current study, we examined the role of polyamines in these effects. Treatment of AR42J cells with the ornithine decarboxylase (ODC) inhibitor difluoromethylornithine (DFMO) inhibited DNA synthesis. Thus polyamines are required for AR42J cell growth. However, we have previously shown that dexamethasone (Dex) increased AR42J cell ODC activity and mRNA levels. In the current study, we found that Dex treatment increased cellular putrescine levels. These increases in ODC and putrescine occurred during Dex-induced inhibition of DNA synthesis. Therefore, in AR42J cells, ODC activity and polyamine levels are not strictly growth related. To examine the requirement for glucocorticoid induction of ODC activity in glucocorticoid stimulation of differentiation, we examined the effects of DFMO on amylase gene expression and cholecystokinin binding. DFMO reduced cell amylase content while having little effect on mRNA levels in both Dex-treated and untreated cells. In contrast, DFMO had little effect on control CCK binding but inhibited the Dex-induced increase. Thus polyamines are necessary for growth and glucocorticoid-induced differentiation of AR42J cells; however, effects of glucocorticoids on AR42J cell growth and differentiation are not mediated by effects on ODC.

scholarly journals Extracellular Na+ and initiation of DNA synthesis: role of intracellular pH and K+.

1984 ◽  
Vol 98 (3) ◽  
pp. 1082-1089 ◽  
Author(s):  
C P Burns ◽  
E Rozengurt
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Dna Synthesis ◽  
Cellular Proliferation ◽  
Weak Acid ◽  
Mechanisms Of Action ◽  
Epidermal Growth ◽  
Reversible Time ◽  
Stimulation Of

Initiation of DNA synthesis in confluent quiescent 3T3 cell cultures stimulated by epidermal growth factor (EGF), vasopressin, and insulin was abolished by removing extracellular Na+. The inhibition was reversible, time- and Na+-concentration-dependent, and not due to an effect on binding or internalization of 125I-EGF. Stimulation by combinations of other growth factors with different mechanisms of action was also affected by decreasing extracellular Na+, but with different half-maximal Na+ concentrations. When choline was used as an osmotic substitute for Na+, the decrease in DNA synthesis was correlated with the decrease in intracellular K+. In contrast, when sucrose was used there was stimulation of the Na+-K+ pump and maintenance of intracellular K+ that resulted in a somewhat higher rate of DNA synthesis at lowered extracellular Na+ compared to choline. Mitogenesis induced by epidermal growth factor, vasopressin, and insulin led to cytoplasmic alkalinization as determined by an increase in uptake of the weak acid 5,5-dimethyloxazolidine-2,4-dione. Experimental decrease in extracellular Na+ blocked this cellular alkalinization. Therefore, under some conditions the supply of extracellular Na+ may limit cellular proliferation because of a reduction in the provision of Na+ to the Na+/H+ antiport and resultant failure of alkalinization. We conclude that Na+ flux and its effect on intracellular K and pH has a major role in the complex system that regulates proliferation.

scholarly journals Graft-vs.-Host Activity of Thymocytes: Relationship to the Role of Thymocytes in Hemopoiesis

Blood ◽  
1972 ◽  
Vol 39 (6) ◽  
pp. 850-861 ◽  
Author(s):  
Joan Wright Goodman ◽  
Kay T. Burch ◽  
Nancy L. Basford
Keyword(s):  
Lymph Node ◽  
F1 Hybrid ◽  
Radiation Chimeras ◽  
Lymph Node Cells ◽  
Per Se ◽  
Uptake Method ◽  
Better Than

Abstract The importance of graft-vs.-host (GVH) activity to the ability of thymocytes to augment hemopoiesis in radiation chimeras was investigated. Parental (P) lymph node cells were found by the 59Fe-uptake method not to have an analogous augmentative effect. When thymus donor, marrow donor, and irradiated recipient were chosen immunogenetically so that GVH could occur in either the presence or absence of graft-vs.-graft (GVG) activity, it was seen that GVH reactivity per se resulted in no improvement of marrow growth. However, when P thymocytes specifically tolerant to an F1 hybrid host were administered with P marrow, augmentation was three times greater than when nontolerant P thymocytes were given. It was concluded that GVH activity not only is not essential but actually is detrimental to augmentation. Ninety-day survival of chimeras given specifically tolerant P thymocytes was better than that of mice given P marrow only and very much better than those given marrow and nontolerant thymocytes.

scholarly journals Stimulation of murine B lymphocytes by isolated C3b.

1975 ◽  
Vol 142 (3) ◽  
pp. 600-610 ◽  
Author(s):  
K U Hartmann ◽  
V A Bokisch
Keyword(s):  
Lymph Node ◽  
Dna Synthesis ◽  
B Lymphocytes ◽  
Cell Cultures ◽  
Fetal Calf Serum ◽  
Calf Serum ◽  
Lymph Node Cell ◽  
Mouse Strains ◽  
Spleen Cells ◽  
Stimulation Of

Addition of isolated B3b to murine lymph node cell cultures induced increased DNA synthesis. The stimulation is dependent on the dose of C3b added and is potentiated by fetal calf serum present in the medium. Isolated C3 is less stimulatory than C3b; C3a and C3c had no effect on DNA synthesis in these cultures. 10-20% large immunoglobulin containing blastlike cells developed in lymph node cell cultures stimulated by 50 mug C3b in the presence of 3% fetal calf serum. The stimulation by C3b was observed in cultures of lymph node and spleen cells of several mouse strains including C3H/HeJ and congenitally thymus-deficient (nu/nu) mice. The results suggest that B lymphocytes are the main target of the stimulatory effect of C3b. Two mechanisms which may be involved in the stimulation of lymphocytes by C3b are discussed: (a) cross-linking of receptors on the cell surface or between cells, and (b) the binding of C3b to receptors of B lymphocytes and the formation of the complement enzyme C3bB. The results are compatible with the suggestion that activation of C3 is part of the events triggering the B lymphocytes.

scholarly journals HAPTEN CARRIER RELATIONSHIPS IN THE DNP-PLL·FOREIGN ALBUMIN COMPLEX SYSTEM: INDUCTION OF TOLERANCE AND STIMULATION OF CELLS IN VITRO

1968 ◽  
Vol 127 (1) ◽  
pp. 43-53 ◽  
Author(s):  
Ira Green ◽  
William E. Paul ◽  
Baruj Benacerraf
Keyword(s):  
Lymph Node ◽  
Cell Cultures ◽  
Thymidine Incorporation ◽  
Lymph Node Cell ◽  
Simple Order ◽  
Significant Stimulation ◽  
Lymph Node Cells ◽  
Stimulate Cell Proliferation ◽  
Stimulation Of

Genetic nonresponder guinea pigs made tolerant to BSA and then immunized with DNP-PLL·BSA failed to make anti-DNP-PLL antibodies. Thus, tolerance to a carrier protein renders animals unresponsive to the hapten which it bears. The addition in vitro of DNP-PLL or DNP-GL to lymph node cell cultures derived from genetic responder animals immunized with these materials led to a significant stimulation of 3H-thymidine incorporation into DNA. However, the addition of DNP-PLL or DNP-GL to lymph node cell cultures from nonresponder animals immunized with these materials failed to produce any stimulation of DNA synthesis. Furthermore, the addition of DNP-PLL to lymph node cell cultures from nonresponder animals immunized with DNP-PLL·BSA or DNP-PLL·OVA also failed to stimulate cell proliferation in spite of the fact that the lymph node cells of these animals were producing anti-DNP-PLL antibodies. The above facts suggest that the function of the PLL gene product is to act at an early crucial step in the immune mechanism to form an antigen-inducer complex. The specificity of this early step may be of a simple order and different than that of the antibody which is later produced in the immune response.

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