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encore19850

銅蟲 (小有名氣)

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[求助] 求助段落中心意思，急急急。大謝。不需要逐字逐句~

CO-SIGNALING MOLECULES AND ANTITUMOR IMMUNITY IN AGING
Co-signaling signals are essential for the augmentation of APC-mediated T cell responses in
antitumor immunity. For example, expression of CD80 (B7.1) and CD86 (B7.2) on APCs or
tumor cells is crucial for promoting antitumor T cell responses.82 Several studies have
demonstrated decreased expression of these co-signaling molecules on aged DCs, which
may contribute to the reduced capacity for T cell stimulation by DCs during aging.73,74
Lustgarten et al. investigated whether CD80 expression on tumor cells was important for the
enhancement of antitumor responses in aged mice. Immunization with the foreign protein
enhanced GFP (EGFP)-expressing BM-185 pre-B-cell lymphoma cells (BM-185-EGFP)
yielded an antitumor immune response in young, but not in aged, mice. However,
immunization with CD80-expressing BM-185-EGFP tumor cells (BM-185-EGFP-CD80)
yielded an antitumor immune response in both young and aged mice, although the tumor
rejection was lower in aged mice compared with young mice.83
There is increasing evidence that several other members of the TNFR family, including
OX40 (CD134), 4-1BB (CD137), CD27, and CD30, may be important as secondary costimulatory
molecules when co-signaling molecules are reduced and insufficient for T cell
stimulation during aging. In studies evaluating the effect of additional OX40 signaling in
antitumor immune responses in aged mice, immunization with BM-185-EGFP-CD80 in
combination with an anti-OX40 mAb markedly improved antitumor response in aged
mice.83 Similarly, an apoptotic tumor cell-pulsed DC vaccine in combination with an anti-
OX40 mAb significantly enhanced the antitumor immune response in aged mice.84
Interestingly, Ruby and Weinberg investigated the efficacy of an anti-OX40 mAb alone in
middle-aged and elderly sarcoma-tumor-bearing mice, and confirmed that the administration
of the mAb to these mice significantly reduced antitumor efficacy because of the decreased
number of differentiated T cells, and was not due to an alteration of the surface expression
of OX40 on T cells.85,86 Furthermore, administration of the anti-OX40 mAb in combination
with IL-12, a cytokine that is essential for T cell differentiation, partially restored the
deficiency in OX40-mediated antitumor efficacy in older mice. 4-1BB is also a member of
the TNFR family that is expressed on activated T cells and co-stimulates both CD4 and CD8
T cells. In particular, Bansal- Pakala and Croft reported that the administration of an agonist
Ab to 4-1BB rescued defective T cell priming in aged mice.87
Similarly, Sharma et al. revealed that apoptotic tumor cell-pulsed DC vaccination in
combination with an anti-4-1BB mAb significantly enhanced the antitumor immune
response in aged mice.84 These results suggest that the insufficient antitumor immune
responses in aging may be restored by the efficient expression of co-stimulatory signals.
V. TLRS AND ANTITUMOR IMMUNITY IN AGING
Recent studies have revealed that innate immune responses and adaptive immune responses
collaborate to induce a strong antitumor immune response. For example, the mediation of
innate immune responses by members of the Toll-like receptor (TLR) family results in the
subsequent induction of protective adaptive immune responses in antitumor immunity.88,89
Several studies have demonstrated that advancing age may affect the expression and
function of TLRs, and the response to TLR ligands in the innate immune system. Renshaw
et al. reported that aged splenic and peritoneal macrophages express significantly lower
levels of TLRs and secrete significantly lower levels of cytokines after stimulation with
various TLR ligands.90 Previous studies have shown that CpG-ODN stimulates
plasmacytoid DCs to produce type I interferons (IFN α and β), which inhibit the synthesis of
Th2 cytokines by CD4 T cells and induce IL-4-inhibited Th1 cells to synthesize IL-2, IL-12,
and IFN-γ. In turn, these induce NK cells, NKT cells, and CTLs in the antitumor immune
responses.91 Sharma et al. reported that the intratumoral injection of CpG-ODN yielded
complete rejection of in vivo tumors in both young and old mice; however, injection of poly
I:C exhibited in vivo tumor rejection only in young mice.92 The authors also revealed that
the induction of the antitumor immune response by in vivo challenge with CpG-ODN, but
not poly I:C in old mice, was correlated with the upregulation of pro-inflammatory cytokine
secretion, significant accumulation of CD4 T cells, CD8 T cells, NK cells, and APCs within
the tumor, and reduction of the number of Tregs within the tumor. These results indicate that
the efficacy of TLR ligands in antitumor immunity may be reduced during the aging
process. Moreover, there is a difference in capacity to induce immune responses among the
various TLR ligands in the old mice.92 It appears that CpG-ODN may constitute a possible
therapeutic approach to overcome the age-associated immune defects in cancer
immunotherapy and restore the antitumor immune response in the elderly.
VI. IMMUNOSUPPRESSIVE CELLS AND ANTITUMOR IMMUNITY IN AGING
Advancing age may alter the prevalence and function of immune suppressive cells such as
CD4+ CD25+FoxP3+ regulatory T cells (Tregs) and myeloid-derived suppressor cells
(MDSCs). Tregs accumulate in tumor-bearing hosts and play fundamental roles in blocking
antitumor immune responses.93,94 MDSCs, a heterogeneous population comprised of
immature myeloid cells, accumulate within sites of cancer, inflammation, and infection,95,96
and have a strong capability to suppress both adaptive and innate immune responses.
Accumulating evidence has revealed that the elimination of either population in a tumorbearing
host may contribute to enhanced antitumor immune responses.
Whereas the age-dependent changes in the number of Tregs and their function remain
controversial, 30 several studies have suggested that Tregs accumulate with age and are
involved in the age-associated immune dysfunction. Gregg et al. reported that the number of
human peripheral blood Tregs increases with age, whereas the function of these cells is
comparable between the young and the old.97 Sharma et al. reported that the increased
frequency of Tregs in aged mice prevented the cytotoxic T cell response in aged tumorbearing
mice.98 Pan et al. also showed that the accumulation of Tregs in aged humans and
mice was closely associated with lung tumor burden.99 Further studies will be required to
test Treg frequency and functions in the periphery versus within the tumor itself, and the
impact on clinical outcome.
Similar to the Tregs, it has been demonstrated that the decline of antitumor T cell function in
aged animal is also correlated with the accumulation of MDSCs with age. Grizzle et al.
revealed that MDSCs are increased in the spleen of aged mice, and that adoptive transfer of
these aged MDSCs delayed tumor rejection significantly in young tumor-bearing mice
Similarly, Sharma et al. revealed that apoptotic tumor cell-pulsed DC vaccination in
combination with an anti-4-1BB mAb significantly enhanced the antitumor immune
response in aged mice.84 These results suggest that the insufficient antitumor immune
responses in aging may be restored by the efficient expression of co-stimulatory signals.
Tomihara et al. Page 5
Crit Rev Oncog. Author manuscript; available in PMC 2014 March 20.
NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript
V. TLRS AND ANTITUMOR IMMUNITY IN AGING
Recent studies have revealed that innate immune responses and adaptive immune responses
collaborate to induce a strong antitumor immune response. For example, the mediation of
innate immune responses by members of the Toll-like receptor (TLR) family results in the
subsequent induction of protective adaptive immune responses in antitumor immunity.88,89
Several studies have demonstrated that advancing age may affect the expression and
function of TLRs, and the response to TLR ligands in the innate immune system. Renshaw
et al. reported that aged splenic and peritoneal macrophages express significantly lower
levels of TLRs and secrete significantly lower levels of cytokines after stimulation with
various TLR ligands.90 Previous studies have shown that CpG-ODN stimulates
plasmacytoid DCs to produce type I interferons (IFN α and β), which inhibit the synthesis of
Th2 cytokines by CD4 T cells and induce IL-4-inhibited Th1 cells to synthesize IL-2, IL-12,
and IFN-γ. In turn, these induce NK cells, NKT cells, and CTLs in the antitumor immune
responses.91 Sharma et al. reported that the intratumoral injection of CpG-ODN yielded
complete rejection of in vivo tumors in both young and old mice; however, injection of poly
I:C exhibited in vivo tumor rejection only in young mice.92 The authors also revealed that
the induction of the antitumor immune response by in vivo challenge with CpG-ODN, but
not poly I:C in old mice, was correlated with the upregulation of pro-inflammatory cytokine
secretion, significant accumulation of CD4 T cells, CD8 T cells, NK cells, and APCs within
the tumor, and reduction of the number of Tregs within the tumor. These results indicate that
the efficacy of TLR ligands in antitumor immunity may be reduced during the aging
process. Moreover, there is a difference in capacity to induce immune responses among the
various TLR ligands in the old mice.92 It appears that CpG-ODN may constitute a possible
therapeutic approach to overcome the age-associated immune defects in cancer
immunotherapy and restore the antitumor immune response in the elderly.
VI. IMMUNOSUPPRESSIVE CELLS AND ANTITUMOR IMMUNITY IN AGING
Advancing age may alter the prevalence and function of immune suppressive cells such as
CD4+ CD25+FoxP3+ regulatory T cells (Tregs) and myeloid-derived suppressor cells
(MDSCs). Tregs accumulate in tumor-bearing hosts and play fundamental roles in blocking
antitumor immune responses.93,94 MDSCs, a heterogeneous population comprised of
immature myeloid cells, accumulate within sites of cancer, inflammation, and infection,95,96
and have a strong capability to suppress both adaptive and innate immune responses.
Accumulating evidence has revealed that the elimination of either population in a tumorbearing
host may contribute to enhanced antitumor immune responses.
Whereas the age-dependent changes in the number of Tregs and their function remain
controversial, 30 several studies have suggested that Tregs accumulate with age and are
involved in the age-associated immune dysfunction. Gregg et al. reported that the number of
human peripheral blood Tregs increases with age, whereas the function of these cells is
comparable between the young and the old.97 Sharma et al. reported that the increased
frequency of Tregs in aged mice prevented the cytotoxic T cell response in aged tumorbearing
mice.98 Pan et al. also showed that the accumulation of Tregs in aged humans and
mice was closely associated with lung tumor burden.99 Further studies will be required to
test Treg frequency and functions in the periphery versus within the tumor itself, and the
impact on clinical outcome.
Similar to the Tregs, it has been demonstrated that the decline of antitumor T cell function in
aged animal is also correlated with the accumulation of MDSCs with age. Grizzle et al.
revealed that MDSCs are increased in the spleen of aged mice, and that adoptive transfer of
these aged MDSCs delayed tumor rejection significantly in young tumor-bearing mice.100
Tomihara et al. Page 6
Crit Rev Oncog. Author manuscript; available in PMC 2014 March 20.
NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript
More recently, the proportion of MDSCs was found to be elevated significantly in elderly
patients with a history of cancer.101
Importantly, a number of pro-inflammatory cytokines that are required for the differentiation
of MDSCs (e.g., TNF-α, IL-6, and IL-1β) are increased in the old,101,102 suggesting that the
age-related inflammatory milieu possibly promotes the accumulation and activation of
MDSCs that subsequently could contribute to the increased aging-associated cancer
incidence. Interestingly, it is possible to note a mutual interaction between the Treg cells and
the MDSCs. In fact, MDSC contributes to Treg induction in cancer, but, in turn, Tregs may
regulate MDSC expansion with a mechanism of positive feedback. In support, our group
reported an age-specific inverse correlation between the prevalence of Tregs and MDSCs.103
We examined the antitumor response to Treg depletion in the B16 melanoma model and
revealed that Treg depletion alone using denileukin diftitox (DT) exerted therapeutic effects
only in young mice but not aged mice. Furthermore, Treg depletion using DT in aged mice
resulted in an increased number of MDSCs. MDSC depletion in combination with Treg
depletion restored the impaired efficacy of Treg depletion in aged mice, suggesting that
Tregs control the prevalence of MDSCs in aged mice and that Treg depletion in combination
with MDSC depletion may be an effective cancer immune therapy approach for the elderly.

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encore19850(RXMCDM代發(fā)): 金幣+10, 多謝應(yīng)助！ 2015-02-01 08:53:54

CO-信號分子和抗腫瘤免疫中的老化
共信令信號是用于APC介導(dǎo)的T細(xì)胞應(yīng)答的增強必不可少
抗腫瘤免疫。例如， CD80 （ B7.1 ）及CD86 （ B7.2 ）對裝甲運兵車的表達(dá)或
腫瘤細(xì)胞是用于促進(jìn)抗腫瘤T細(xì)胞responses.82幾項研究有關(guān)鍵
表現(xiàn)在減少老年的DC ，這些共同信號分子的表達(dá)，這
在aging.73,74可能有助于T細(xì)胞刺激樹突狀能力下降
勒斯特加滕等。調(diào)查了在腫瘤細(xì)胞上的CD80表達(dá)是否是重要的
增強老年小鼠的抗腫瘤反應(yīng)。接種外源蛋白
增強的GFP （綠色熒光蛋白） -expressing BM- 185的前B細(xì)胞淋巴瘤細(xì)胞（BM -185 -EGFP ）
產(chǎn)生在年輕的抗腫瘤免疫反應(yīng)，但不是在老年小鼠。然而，
免疫CD80表達(dá)的BM- 185 -EGFP腫瘤細(xì)胞（BM -185 -EGFP- CD80 ）
在取得了年輕和老年小鼠的抗腫瘤免疫反應(yīng)，雖然腫瘤
抑制明顯低于老年小鼠與年輕mice.83比較
有越來越多的證據(jù)表明，腫瘤壞死因子受體家族的其他幾個成員，包括
OX40 （ CD134 ）， 4-1BB （ CD137 ）， CD27 ，和CD30，可能是重要的，因為輔助共刺激
分子時共信號分子被減少和不足的T細(xì)胞
老化過程中的刺激。在研究評估更多的OX40信號的影響
在老年小鼠的抗腫瘤免疫應(yīng)答，免疫BM- 185 -EGFP- CD80在
與老年抗OX40單抗顯著改善的抗腫瘤反應(yīng)的組合
mice.83類似地，在組合的凋亡腫瘤細(xì)胞致敏的DC疫苗與抗
OX40單抗顯著提高老年mice.84的抗腫瘤免疫反應(yīng)
有趣的是， Ruby和溫伯格調(diào)查的抗OX40單抗的療效獨
中年和老年肉瘤荷瘤小鼠，并證實該管理
單克隆抗體對這些小鼠顯著減少由于減少抗腫瘤功效
號分化T細(xì)胞的，并且不是由于表面表達(dá)的改變
OX40對T cells.85,86此外，抗OX40單抗的施用組合
與IL- 12，細(xì)胞因子，是用于T細(xì)胞分化所必需的，部分還原的
不足OX40介導(dǎo)的抗腫瘤效果在老年小鼠。 4-1BB也是一個構(gòu)件
被表達(dá)在活化的T細(xì)胞和共能刺激CD4和CD8的TNFR家族
T細(xì)胞。特別是， Bansal- Pakala和克羅夫特報道，激動劑的給藥
AB公司4-1BB救出缺陷的T細(xì)胞引發(fā)老年mice.87
同樣， Sharma等。發(fā)現(xiàn)在細(xì)胞凋亡的腫瘤細(xì)胞致敏的DC疫苗接種
用抗4-1BB組合MAB顯著增強了抗腫瘤免疫
響應(yīng)老年mice.84這些結(jié)果表明，在不充分的抗腫瘤免疫
在老化的反應(yīng)可通過共刺激信號的有效表達(dá)恢復(fù)。
五， TLRS和抗腫瘤免疫中的老化
最近的研究表明，先天免疫應(yīng)答和適應(yīng)性免疫反應(yīng)
協(xié)作，以誘導(dǎo)強的抗腫瘤免疫應(yīng)答。例如，中介
由Toll樣受體的成員（TLR）家族導(dǎo)致先天免疫反應(yīng)
隨后誘導(dǎo)抗腫瘤immunity.88,89保護(hù)性免疫反應(yīng)
幾項研究已經(jīng)表明，年齡增長可能會影響表達(dá)和
功能的TLR的，并且在先天免疫系統(tǒng)對TLR配體的應(yīng)答。倫肖
等。報道稱，中年脾及腹腔巨噬細(xì)胞表達(dá)顯著降低
TLR的水平，以及刺激后分泌的細(xì)胞因子的顯著較低水平
不同的TLR ligands.90以往的研究表明，的CpG -ODN可以刺激
漿的DCs產(chǎn)生的I型干擾素（干擾素α和β ），其抑制的合成
通過CD4T細(xì)胞Th2細(xì)胞因子并誘導(dǎo)IL-4抑制Th1細(xì)胞合成IL-2， IL-12，
和IFN-γ 。反過來，這些誘導(dǎo)NK細(xì)胞， NKT細(xì)胞，和的CTL在抗腫瘤免疫
responses.91 Sharma等。報道稱，瘤內(nèi)注射的CpG -ODN墓內(nèi)
在體內(nèi)腫瘤的年輕和年老小鼠完全拒絕;然而，注射聚
I：C展出體內(nèi)腫瘤排斥只有在年輕的mice.92作者還透露，
誘導(dǎo)通過體內(nèi)挑戰(zhàn)與CpG的寡核苷酸的抗腫瘤免疫應(yīng)答的，但
不聚I：C在老年小鼠，率與促炎癥細(xì)胞因子的表達(dá)上調(diào)
分泌， CD4 + T細(xì)胞的顯著積累， CD8 + T細(xì)胞內(nèi)，NK細(xì)胞，和的APC
腫瘤，和減少的Treg的腫瘤內(nèi)的數(shù)目。這些結(jié)果表明
TLR的配體功效的抗腫瘤免疫的老化過程中可減少
流程。此外，有在容量的差，以誘發(fā)其中的免疫應(yīng)答
各種TLR配體的老mice.92似乎的CpG -ODN可構(gòu)成一個可能的
治療方法，以克服在癌癥中的年齡相關(guān)的免疫缺陷
免疫治療和恢復(fù)中老年人的抗腫瘤免疫反應(yīng)。
VI 。免疫抑制細(xì)胞和抗腫瘤免疫中的老化
年齡的增長可能會改變免疫抑制細(xì)胞如患病率和功能
CD4 + CD25 + Foxp3 +調(diào)節(jié)性T細(xì)胞（ Treg細(xì)胞）和骨髓源性抑制細(xì)胞
（肌源性干細(xì)胞）。調(diào)節(jié)性T細(xì)胞積聚在腫瘤攜帶主機和發(fā)揮基本作用在阻斷
抗腫瘤免疫responses.93,94的MDSCs ，異質(zhì)群體包括
未成熟髓樣細(xì)胞，積聚的癌癥，炎癥和感染， 95,96位點內(nèi)
并且有很強的能力，同時抑制適應(yīng)性和先天免疫反應(yīng)。
越來越多的證據(jù)顯示，消除任何人口中荷瘤
主機可能有助于增強抗腫瘤免疫應(yīng)答。
而在調(diào)節(jié)性T細(xì)胞的數(shù)目的年齡依賴性的變化和它們的功能保持
有爭議的， 30幾個研究已經(jīng)表明，調(diào)節(jié)性T細(xì)胞積累與年齡，是
參與年齡相關(guān)的免疫功能紊亂。格雷格等。報道稱，數(shù)
人外周血Treg細(xì)胞隨著年齡的增加，而這些細(xì)胞的功能是
可比的年輕人和old.97夏爾馬等人之間。報告說，增加的
調(diào)節(jié)性T細(xì)胞在老年小鼠的頻率防止老年荷瘤的細(xì)胞毒性T細(xì)胞反應(yīng)
mice.98 Pan等。還表明，調(diào)節(jié)性T細(xì)胞的老年人的積累和
小鼠緊密burden.99進(jìn)一步的研究將要求肺腫瘤相關(guān)
測試的Treg頻率和功能，在周邊部與腫瘤本身內(nèi)，并且
對臨床結(jié)果的影響。
類似的Treg ，它已被證明的抗腫瘤T細(xì)胞功能中的下降
老年動物也與肌源性干細(xì)胞隨著年齡的積累�；疑取�
透露，肌源性干細(xì)胞在老年小鼠的脾增大，而繼轉(zhuǎn)讓
這些年齡肌源性干細(xì)胞延緩腫瘤抑制顯著年輕荷瘤mice.100
Tomihara等。第6頁
暴擊牧師Oncog 。作者的手稿;可在2014年P(guān)MC 3月20日。
NIH -PA作者手稿NIH -PA作者手稿NIH -PA作者手稿
最近，肌源性干細(xì)胞的比例被認(rèn)為是老年顯著升高
患者cancer.101史
重要的是，許多促炎細(xì)胞因子的所需要的分化
肌源性干細(xì)胞（例如， TNF-α， IL-6和IL-1β ），在舊的增加， 101102提示
年齡相關(guān)的炎癥環(huán)境可能促進(jìn)的積累和活化
肌源性干細(xì)胞在此之后可有助于增加衰老相關(guān)癌癥
發(fā)病率。有趣的是，有可能要注意的Treg細(xì)胞和之間的相互作用
該肌源性干細(xì)胞。事實上， MDSC有助于Treg細(xì)胞的誘導(dǎo)在癌癥，但反過來，調(diào)節(jié)性T細(xì)胞可
規(guī)范MDSC擴張與正反饋的機制。在支持，我們的團隊
報道調(diào)節(jié)性T細(xì)胞和MDSCs.103的患病率之間的特定年齡呈負(fù)相關(guān)
我們審查了黑色素瘤模型中的抗腫瘤反應(yīng)調(diào)節(jié)性T細(xì)胞耗竭和
透露，調(diào)節(jié)性T細(xì)胞耗竭單獨使用尼白介素（ DT ）發(fā)揮治療作用
只有在年輕的小鼠，但不是老年小鼠。此外，在老年小鼠使用DT調(diào)節(jié)性T細(xì)胞耗竭
導(dǎo)致的MDSCs的數(shù)量增加。 MDSC枯竭與調(diào)節(jié)性T細(xì)胞結(jié)合
枯竭恢復(fù)Treg細(xì)胞耗竭的療效受損老年小鼠，這表明
調(diào)節(jié)性T細(xì)胞控制肌源性干細(xì)胞的患病率在老年小鼠和調(diào)節(jié)性T細(xì)胞耗竭組合
同的MDSC枯竭可能是老年人的有效的癌癥免疫治療的方法。

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