Production of and in vitro response to interleukin 2 in the acquired immunodeficiency syndrome.
Production of and in vitro response to interleukin 2 in the acquired immunodeficiency syndrome.
复制标题
获得性免疫缺陷综合征中白细胞介素 2 的产生和体外反应。
DOI:
10.1172/jci112194
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发表时间:
1985
期刊:
影响因子:
--
通讯作者:
Roberts,RB
中科院分区:
文献类型:
--
作者:
Murray,HW;Welte,K;Jacobs,JL;Rubin,BY;Mertelsmann,R;Roberts,RB
To test the hypothesis that deficient interleukin 2 (IL-2) secretion may underlie the impaired capacity of T cells from patients with Acquired Immunodeficiency Syndrome (AIDS) and the AIDS-related complex (ARC) to generate the macrophage-activating lymphokine, gamma interferon (IFN-gamma), we used five specific microbial antigens to examine IL-2 production. Mononuclear cells from only one of 32 (3%) AIDS patients secreted normal levels of IL-2, and 21 (66%) failed to produce any detectable IL-2. For 36 ARC patients, IL-2 generation was normal in nine (25%) and absent in 11 (31%). Given these results, recombinant (r) IL-2 was tested for its capacity to stimulate or enhance IFN-gamma production. rIL-2 (10 U/ml) alone stimulated cells from controls, ARC, and AIDS patients to secrete 93 +/- 25, 99 +/- 33, and 7 +/- 3 U/ml of IFN-gamma, respectively. rIL 2 (10 U/ml) plus antigen induced no change in mean IFN-gamma levels for controls, a 4.4-fold increase for 17 AIDS patients (16 +/- 16 vs. 71 +/- 21 U/ml), and a 7.2-fold increase (18 +/- 5 vs. 130 +/- 27 U/ml) for 19 ARC patients with abnormal IFN-gamma generation to antigen alone. Individual responses indicated that six of the 17 (35%) AIDS patients with opportunistic infections and 12 of the 19 (63%) with ARC were apparent responders to 10-100 U/ml of rIL-2. These results (a) document profound impairment in antigen-induced IL-2 secretion by AIDS and ARC T cells, (b) indicate that, in vitro, mononuclear cells from certain patients can respond to rIL-2 with enhanced IFN-gamma production, and thus (c) suggest that in selected patients rIL-2 might have a potentially beneficial therapeutic (AIDS) or prophylactic (ARC) effect against opportunistic infections.
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影响因子:
3.1
作者:
C. Nacy;S. James;W. Benjamin;JOHiN J. Farrar;W. Hockmeyer;M. Meltzer;A. C.;Nacy;A. Fortier;M. G. Pappas
通讯作者:
M. G. Pappas
影响因子:
4.4
作者:
A. Rook;J. Hooks;G. Quinnan,;H. Lane;J. Manischewitz;A. Macher;H. Masur;A. Fauci;J. Djeu
通讯作者:
J. Djeu
影响因子:
4.4
作者:
W. Farrar;H. Johnson;J. Farrar
通讯作者:
J. Farrar
影响因子:
4.4
作者:
B. Torres;W. Farrar;H. Johnson
通讯作者:
H. Johnson
DOI:
--
发表时间:
1984
影响因子:
11.1
作者:
T. Chang;S. McKinney;V. Liu;P. Kung;J. Vilček;J. Le
通讯作者:
J. Le