High numbers of programmed cell death-1-positive tumor infiltrating lymphocytes correlate with early onset of post-transplant lymphoproliferative disorder
High numbers of programmed cell death-1-positive tumor infiltrating lymphocytes correlate with early onset of post-transplant lymphoproliferative disorder
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大量程序性细胞死亡 1 阳性肿瘤浸润淋巴细胞与移植后淋巴细胞增殖性疾病的早期发病相关
DOI:
10.1007/s12185-021-03129-3
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发表时间:
2021
影响因子:
2.1
通讯作者:
Ohshima Koichi
中科院分区:
文献类型:
--
作者:
Saito Hideaki;Miyoshi Hiroaki;Shibayama Hirohiko;Toda Jun;Kusakabe Shinsuke;Ichii Michiko;Fujita Jiro;Fukushima Kentaro;Maeda Tetsuo;Mizuki Masao;Oritani Kenji;Seto Masao;Yokota Takafumi;Kanakura Yuzuru;Hosen Naoki;Ohshima Koichi
Post-transplant lymphoproliferative disorder (PTLD) is a life-threatening complication of transplantation. In addition to reactivation of Epstein–Barr virus in immunocompromised patients, impaired tumor immunity is suggested to be a risk factor for PTLD. However, it remains unclear whether immune suppressive tumor-infiltrating lymphocytes (TILs) correlate with the occurrence or prognosis of PTLD. We analyzed TILs in 26 patients with PTLD to elucidate the clinicopathological significance of the expression of PD-1 and FoxP3, which are associated with exhausted T-cells and regulatory T-cells (Tregs), respectively. Numbers of PD-1+TILs in the PTLD specimens were significantly higher in patients who developed PTLD early after transplantation (P= 0.0040), while numbers of FoxP3+TILs were not (P= 0.184). There was no difference in overall response rate regardless of the expression of PD-1 or FoxP3. FoxP3highpatients tended to have a shorter time to progression compared with FoxP3lowpatients, especially in the case of FoxP3highpatients with diffuse large B-cell lymphoma-subtype PTLD (P= 0.011), while PD-1highpatients did not. These results suggest that T-cell exhaustion may be mainly associated with PTLD development, while immune suppression by Tregs may be dominant in enhanced progression of PTLD following disease occurrence.
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影响因子:
10.1
作者:
S. Choquet;R. Trappe;V. Leblond;U. Jäger;F. Davi;S. Oertel
通讯作者:
S. Oertel
影响因子:
6.2
作者:
Martinez OM;Krams SM
通讯作者:
Krams SM
影响因子:
6.2
作者:
D. Berglund;A. Kinch;Elin Edman;C. Backlin;G. Enblad;E. Larsson;D. Molin;K. Pauksens;C. Sundström;E. Baecklund
通讯作者:
E. Baecklund
DOI:
10.1056/nejmoa1200694
发表时间:
2012-06-28
期刊:
The New England journal of medicine
影响因子:
--
作者:
Brahmer JR;Tykodi SS;Chow LQ;Hwu WJ;Topalian SL;Hwu P;Drake CG;Camacho LH;Kauh J;Odunsi K;Pitot HC;Hamid O;Bhatia S;Martins R;Eaton K;Chen S;Salay TM;Alaparthy S;Grosso JF;Korman AJ;Parker SM;Agrawal S;Goldberg SM;Pardoll DM;Gupta A;Wigginton JM
通讯作者:
Wigginton JM
影响因子:
45.3
作者:
Lesokhin, Alexander M.;Ansell, Stephen M.;Timmerman, John
通讯作者:
Timmerman, John