Appearance of cytokine-associated central nervous system myelin damage coincides temporally with serum tumor necrosis factor induction after recombinant interleukin-2 infusion in rats

1991 ◽  
Vol 33 (3) ◽  
pp. 245-251 ◽  
Author(s):  
Mary D. Ellison ◽  
Randall E. Merchant
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Interleukin 2 ◽  
Recombinant Interleukin 2 ◽  
Tumor Necrosis Factor Induction ◽  
Necrosis Factor ◽  
Serum Tumor Necrosis ◽  
Myelin Damage

Tumor necrosis factor facilitates regeneration of injured central nervous system axons

1991 ◽  
Vol 545 (1-2) ◽  
pp. 334-338 ◽  
Author(s):  
M. Schwartz ◽  
A. Solomon ◽  
V. Lavie ◽  
S. Ben-Bassat ◽  
M. Belkin ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Necrosis Factor

scholarly journals Homeostatic action of interleukin-4 on endogenous and recombinant interleukin-2-induced activated killer cell function

Blood ◽  
1991 ◽  
Vol 77 (6) ◽  
pp. 1283-1289
Author(s):  
C Bello-Fernandez ◽  
C Bird ◽  
HE Heslop ◽  
DJ Gottlieb ◽  
JE Reittie ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Marrow Transplantation ◽  
Tumor Necrosis ◽  
Cell Function ◽  
Interleukin 2 ◽  
Gamma Interferon ◽  
Target Cells ◽  
Recombinant Interleukin 2 ◽  
Necrosis Factor

Cytokine-secreting, major histocompatibility complex-unrestricted activated killer (AK) cells are toxic to a wide range of virus-infected or malignant target cells and may be generated endogenously, eg, after bone marrow transplantation, or by infusion of cytokines such as recombinant interleukin-2 (rIL-2). Although AK cells secrete cytokines such as gamma-interferon and tumor necrosis factor, which are themselves able to recruit fresh cytokine-secreting AK cells, activation in both settings is short-lived, implying the existence of homeostatic regulatory mechanisms. We now demonstrate one mechanism by which rapid homeostasis is achieved. We show that IL-4 is produced in patients with both endogenously and exogenously generated AK cells. The cytokine was detected in serum after marrow transplantation, and IL-4 transcripts appeared in circulating lymphocytes during rIL-2 infusion. Although IL-4 inhibited the induction phase of AK cell function, it had no significant inhibitory effect on the ability of AK cells from these individuals to respond to restimulation. Nonetheless, neutralization of the IL-4 induced during cell activation doubled the half-life of AK function, once activating stimuli were removed, from 18 to 44 hours and produced a 2-log increase in AK cell secretion of tumor necrosis factor and gamma-interferon. These data suggest that IL-4 induced in vivo during lymphocyte activation abbreviates AK cell responses once the triggering stimuli have been removed. Neutralization of endogenous IL-4 in vivo by appropriate monoclonal antibodies might prolong the duration of AK function.

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