本文選題：重癥肺炎　切入點(diǎn)：免疫無(wú)能　出處：《廣州醫(yī)學(xué)院》2009年碩士論文

【摘要】： 背景 重癥肺炎目前具體的發(fā)病機(jī)制不詳。研究發(fā)現(xiàn)重癥肺炎患者淋巴細(xì)胞顯著減少,并與患者的預(yù)后密切相關(guān)。是什么導(dǎo)致重癥肺炎淋巴細(xì)胞減少?研究表明重癥肺炎患者外周血中協(xié)同刺激分子表達(dá)異常,可能導(dǎo)致T淋巴細(xì)胞處于“免疫無(wú)能(anergy)”狀態(tài)。其中是因?yàn)門淋巴細(xì)胞相關(guān)的協(xié)同刺激分子CD28,CD152及CD86等的表達(dá)異常,還是因?yàn)镃D28/CD152這對(duì)相互拮抗的信號(hào)分子的比例異常導(dǎo)致了T淋巴細(xì)胞處于“免疫無(wú)能”狀態(tài)?目前尚不清楚。研究發(fā)現(xiàn)胸腺肽-α1(Tα1)在機(jī)體免疫應(yīng)答過(guò)程中起著重要的作用,并認(rèn)為其可能是通過(guò)增強(qiáng)T淋巴細(xì)胞功能而調(diào)節(jié)免疫系統(tǒng)的。研究觀察到胸腺肽a1可以改善膿毒性休克患者的T淋巴細(xì)胞增殖,調(diào)節(jié)機(jī)體的細(xì)胞免疫功能�？梢�(jiàn),胸腺肽a1有調(diào)節(jié)機(jī)體免疫異常的功能,是否通過(guò)調(diào)控協(xié)同刺激信號(hào)來(lái)影響T淋巴細(xì)胞的增殖?尚待進(jìn)一步的研究。 目的 在蛋白水平上研究重癥肺炎T細(xì)胞相關(guān)協(xié)同刺激分子與其細(xì)胞增殖能力的關(guān)系,以探討該病的發(fā)病機(jī)制;在此基礎(chǔ)上,觀察胸腺肽-α1對(duì)重癥肺炎T淋巴細(xì)胞協(xié)同刺激分子及其細(xì)胞增殖能力的影響,并進(jìn)一步探討T淋巴細(xì)胞協(xié)同刺激分子在重癥肺炎免疫異常中的可能作用。 資料和方法 1標(biāo)本來(lái)源 2007年8月一2008年06月入住廣州市第一人民醫(yī)院呼吸科的重癥肺炎患者,均符合美國(guó)胸科學(xué)會(huì)(ATS)于2007年制定的重癥肺炎診斷標(biāo)準(zhǔn)。健康對(duì)照組來(lái)自同期門診健康體檢者。經(jīng)本人及家屬知情同意后抽取外周靜脈血。重癥肺炎患者21例,抽血2mL,EDTA-K3抗凝;其中11例多抽血13mL,肝素抗凝;另外其中11例于住院治療后10天再次抽血2mL(其中28天患者預(yù)后為8例好轉(zhuǎn)、3例死亡)。健康人12名抽血2mL,EDTA-K3抗凝;其中10名多抽血8mL肝素抗凝。 2方法 2.1 T淋巴細(xì)胞相關(guān)協(xié)同刺激分子的檢測(cè):取EDTA-K3抗凝血標(biāo)本。設(shè)測(cè)定管及同型對(duì)照管。檢測(cè)T淋巴細(xì)胞上的四個(gè)表位(CD4, CD8, CD28, CD152)及相關(guān)的單核細(xì)胞的兩個(gè)表位(CD86,HLA-DR)。用FITC、PE、PC5、APC和APCcy7熒光素直接標(biāo)記單克隆抗體。檢測(cè)前校準(zhǔn)流式細(xì)胞儀的光路和液路。將光路調(diào)整至最佳,檢測(cè)陰性對(duì)照,調(diào)整電壓和顏色補(bǔ)償。利用FACScan及CELLQuest軟件收集分析數(shù)據(jù)。使用前向角散射光側(cè)向角散射光雙參數(shù)設(shè)門。收集10000個(gè)細(xì)胞。以百分率表示每群細(xì)胞的表達(dá)。 2.2 T淋巴細(xì)胞的增殖試驗(yàn) 2.2.1人外周血單個(gè)核細(xì)胞(PBMC)提取:密度梯度離心法提取重癥肺炎病人及健康人的外周血標(biāo)本(PBMC)。立即使用或凍存,用前溶解。 2.2.2單個(gè)核細(xì)胞(PBMC)PKH26染色及培養(yǎng):參考PKH26染料說(shuō)明書對(duì)PBMC進(jìn)行染色。重懸成1×106 / ml的濃度,接種于24孔培養(yǎng)板孔中。實(shí)驗(yàn)分為4組:①空白對(duì)照組PBS+PKH26染色后PBMC;②陽(yáng)性對(duì)照組PHA+PKH26染色后PBMC;③胸腺肽-α1+內(nèi)毒素+PKH26染色后PBMC;④內(nèi)毒素PKH26+染色后PBMC。每孔終體積約0.6 ml濃度1×106 / ml,在37℃、5 %CO2條件下培養(yǎng)5天。 2.2.3 T淋巴細(xì)胞增殖的檢測(cè):取出培養(yǎng)5天后的PKH26染色細(xì)胞,分兩管,每管0.3ml ,離心洗滌,加入熒光素標(biāo)記的PC5—CD3 1μg/ 106細(xì)胞,混勻后室溫暗處孵育,洗滌后,用2 g/L多聚甲醛固定,利用流式細(xì)胞儀檢測(cè)及數(shù)據(jù)用CELLQuest軟件和ModFitTM軟件分析得到T淋巴細(xì)胞的增殖指數(shù)(PF)及增殖細(xì)胞的前體頻率(PI)。 2.2.4體外培養(yǎng)T淋巴細(xì)胞及協(xié)同分子的檢測(cè):取未染色的單個(gè)核細(xì)胞,重懸成1×106 / ml的濃度,接種于24孔培養(yǎng)板孔中。實(shí)驗(yàn)分為4分組:①空白對(duì)照組PBS+未染色PBMC;②陽(yáng)性對(duì)照組PHA+未染色PBMC;③胸腺肽-α1+內(nèi)毒素+未染色PBMC;④內(nèi)毒素+未染色PBMC。每孔終體積約0.6 ml,濃度1×106 / ml,在37℃、5 %CO 2條件下培養(yǎng)5天。取出培養(yǎng)5天后未染色的細(xì)胞,分兩管,每管0.3ml ,離心洗滌,加入熒光素標(biāo)記的FITC—CD28/PE—CD152/PC5—CD3各1μg/ 106細(xì)胞,混勻后室溫暗處孵育,洗滌后,用2 g/L多聚甲醛固定,利用流式細(xì)胞儀檢測(cè)及數(shù)據(jù)用CELLQuest軟件分析協(xié)同刺激分子CD28、CD152的表達(dá)。 2.3統(tǒng)計(jì)學(xué)方法:所有實(shí)驗(yàn)數(shù)據(jù)均用SPSS 11.5軟件分析,計(jì)量資料以均數(shù)士標(biāo)準(zhǔn)差(士S)表示,兩組均數(shù)比較采用t檢驗(yàn)。隨機(jī)區(qū)組設(shè)計(jì)資料采用方差分析,用LSD法進(jìn)行數(shù)據(jù)間的多重比較,取P0.05差異有統(tǒng)計(jì)學(xué)意義。 結(jié)果 1重癥肺炎T淋巴細(xì)胞、亞群及相關(guān)協(xié)同刺激分子:21例重癥肺炎患者CD3、CD4、CD86、HLA-DR、CD28/ CD152、CD4/CD8較12例健康對(duì)照組減少,有統(tǒng)計(jì)學(xué)顯著性差異(P 0.05);CD8、CD28,CD152表達(dá)較健康對(duì)照組增加,有統(tǒng)計(jì)學(xué)顯著性差異(P 0.05)。 2 28天存活組重癥肺炎患者治療前后(10天)T淋巴細(xì)胞、亞群及相關(guān)協(xié)同刺激分子的變化:存活組8例重癥肺炎入院第10天和第1天比較APACHEⅡ評(píng)分顯著減少(P=0.000);CD28、CD152、CD86、HLA-DR的表達(dá)顯著升高(P 0.05);CD3T細(xì)胞也顯著增加(P=0.030);CD8CD3,CD4CD3陽(yáng)性的T細(xì)胞無(wú)顯著變化(P 0.05)。 3 PKH26標(biāo)記重癥肺炎患者外周血單個(gè)核細(xì)胞(PMBC)的情況: PKH26標(biāo)記PMBC,在直方圖上PKH26熒光強(qiáng)度出現(xiàn)明顯右偏,達(dá)104,呈單峰,陽(yáng)性率為96.48%。熒光顯微觀察PKH26標(biāo)記后的PMBC,可見(jiàn)其細(xì)胞發(fā)紅色熒光。 4重癥肺炎患者外周血T淋巴細(xì)胞對(duì)抗原刺激的增殖能力:10例重癥肺炎患者外周血T淋巴細(xì)胞對(duì)內(nèi)毒素(LPS)刺激的增殖指數(shù)PI(1.55±0.42)與增殖細(xì)胞的前體頻率PF(0.02±0.01)低于10例健康人組的PI (2.15±0.29)與PF(0.04±0.02),有統(tǒng)計(jì)學(xué)差異(P 0.05)。 5胸腺肽-α1對(duì)重癥肺炎外周血T淋巴細(xì)胞增殖的影響 5.1光學(xué)顯微鏡觀察胸腺肽-α1對(duì)重癥肺炎外周血T淋巴細(xì)胞增殖的影響:不同干預(yù)因素組重癥肺炎外周血T淋巴細(xì)胞在體外培養(yǎng)5天后,用顯微鏡觀察(×10倍),可見(jiàn)PHA組及胸腺肽-α1加內(nèi)毒素組出現(xiàn)明顯的淋巴細(xì)胞母細(xì)胞化,其他兩組未見(jiàn)明顯的淋巴細(xì)胞母細(xì)胞化。 5.2胸腺肽-α1對(duì)重癥肺炎外周血T淋巴細(xì)胞增殖的影響:10例重癥肺炎PHA組、胸腺肽-α1加內(nèi)毒素組及內(nèi)毒素組T淋巴細(xì)胞的增殖細(xì)胞的前體頻率(PF)分別為:0.03±0.03、0.03±0.02、0.02±0.01;T淋巴細(xì)胞的增殖指數(shù)(PI)分別為:1.68±0.49、1.84±0.53、1.55±0.42。胸腺肽-α1加內(nèi)毒素組T淋巴細(xì)胞的增殖指數(shù)與增殖細(xì)胞的前體頻率比內(nèi)毒素組的高,有統(tǒng)計(jì)學(xué)顯著性差異(P 0.05);胸腺肽-α1加內(nèi)毒素組T淋巴細(xì)胞的增殖指數(shù)及增殖細(xì)胞的前體頻率與PHA組的比較,無(wú)統(tǒng)計(jì)學(xué)顯著性差異(P 0.05)。 6胸腺肽-α1對(duì)重癥肺炎外周血T淋巴細(xì)胞協(xié)同刺激分子的影響 6.1胸腺肽-α1對(duì)重癥肺炎外周血T淋巴細(xì)胞CD28協(xié)同刺激分子的影響: PBS組(67.40±6.45)%、PHA組(72.21±7.05)%、胸腺肽-α1加內(nèi)毒素組(73.70±8.66)%及內(nèi)毒素組(66.94±11.85) %。胸腺肽-α1加內(nèi)毒素組T淋巴細(xì)胞CD28協(xié)同刺激分子的表達(dá)比內(nèi)毒素組及PBS組的高,有統(tǒng)計(jì)學(xué)顯著性差異(P 0.05);胸腺肽-α1加內(nèi)毒素組T淋巴細(xì)胞CD28協(xié)同刺激分子的表達(dá)與PHA組的比較,無(wú)統(tǒng)計(jì)學(xué)顯著性差異(P=0.479)。 6.2胸腺肽-α1對(duì)重癥肺炎外周血T淋巴細(xì)胞CD152協(xié)同刺激分子的影響: PBS組(3.01±1.08)%、PHA組(2.69±1.23)%、胸腺肽-α1加內(nèi)毒素組(2.41±0.77)%及內(nèi)毒素組(2.86±1.03) %。胸腺肽-α1加內(nèi)毒素組T淋巴細(xì)胞CD152協(xié)同刺激分子的表達(dá)比內(nèi)毒素組及PBS組的低,有統(tǒng)計(jì)學(xué)顯著性差異(P 0.05);胸腺肽-α1加內(nèi)毒素組T淋巴細(xì)胞CD152協(xié)同刺激分子的表達(dá)與PHA組的比較,無(wú)統(tǒng)計(jì)學(xué)顯著性差異(P=0.306)。 6.3胸腺肽-α1對(duì)重癥肺炎外周血T淋巴細(xì)胞協(xié)同刺激分子CD28/CD152比值的影響: PBS組(25.26±9.57)、PHA組(31.38±11.67)、胸腺肽-α1加內(nèi)毒素組(33.30±9.96)及內(nèi)毒素組(21.13±5.39)。胸腺肽-α1加內(nèi)毒素組T淋巴細(xì)胞協(xié)同刺激分子CD28/CD152的比值比內(nèi)毒素組及PBS組的大,有統(tǒng)計(jì)學(xué)顯著性差異(P 0.05);胸腺肽-α1加內(nèi)毒素組T淋巴細(xì)胞協(xié)同刺激分子CD28/CD152的比值與PHA組的比較,無(wú)統(tǒng)計(jì)學(xué)顯著性差異(P=0.490)。 結(jié)論 1.重癥肺炎患者外周血T淋巴細(xì)胞存在“免疫無(wú)能”,導(dǎo)致了T淋巴細(xì)胞及CD4亞群減少,抑制了機(jī)體的免疫功能。 2. T淋巴細(xì)胞相關(guān)協(xié)同刺激分子CD28、CD152及CD86表達(dá)異常參與了重癥肺炎發(fā)病的病理生理過(guò)程。 3.體外胸腺肽-α1可通過(guò)調(diào)節(jié)重癥肺炎患者外周血T淋巴細(xì)胞協(xié)同刺激分子CD28、CD152表達(dá);來(lái)改善其對(duì)抗原刺激的增殖能力。
[Abstract]:background
At present, the specific pathogenesis of severe pneumonia is unknown. The study found that lymphocytes of patients with severe pneumonia was significantly reduced, and is closely related to the prognosis of the patients. What caused the reduction of lymphocytes? Study showed that patients with severe pneumonia in the peripheral blood of abnormal expression of costimulatory molecules, may lead to T lymphocytes in immune incompetence (anergy) ". One is because the T lymphocyte associated costimulatory molecules CD28, expression of CD152 and CD86 anomalies, or because the CD28/CD152 of antagonistic signaling molecules leads to the abnormal rate of T lymph cells in immune incompetent"? Is unclear. The study found that thymosin alpha 1 (T alpha 1) plays an important the role during the immune response, and it may regulate the immune system by enhancing the function of T lymphocytes and the study observed. Thymosin A1 can improve The proliferation of T lymphocytes in patients with septic shock and the regulation of cellular immune function can be seen. Thymosin A1 has the function of regulating the immune abnormality. Whether we need to regulate the co stimulatory signal to affect the proliferation of T lymphocytes remains to be further studied.
objective
Study on the relationship between severe pneumonia T cells at the protein level associated costimulatory molecules and cell proliferation, to investigate the pathogenesis of the disease; on this basis, to observe the effect of thymosin alpha 1 on severe pneumonia in T lymphocytes and cell proliferation, and to further explore the T lymphocytes in immune severe pneumonia the possible role of abnormal.
Information and methods
1 source of specimen
In August 2007 2008 06 a month in the Department of respiration of Guangzhou No.1 People's Hospital of the patients with severe pneumonia, are in line with the American Thoracic Society (ATS) in diagnosis of severe pneumonia standard enacted in 2007. The healthy control group from healthy subjects served by themselves and their families. Informed consent from peripheral venous blood. 21 cases of patients with severe pneumonia, blood 2mL, EDTA-K3 anticoagulant of which 11 cases of multiple blood 13mL; heparin; in addition, of which 11 cases in the hospital 10 days after treatment were 2mL (28 days for the prognosis of patients with 8 cases improved, 3 cases died). 12 healthy people were 2mL, EDTA-K3 anticoagulation; including 10 more blood 8mL heparin.
2 method
2.1 the detection of T lymphocyte associated costimulatory molecules: take EDTA-K3 anticoagulant samples. Test tubes and control tube. The detection of T lymphocyte on the four epitopes (CD4, CD8, CD28, CD152) and mononuclear cells of two epitopes (CD86, HLA-DR). FITC, PE PC5, directly labeled monoclonal antibody APC and APCcy7 fluorescein. Before testing, calibration of flow cytometry light path and liquid. The light path adjustment to the best detection, negative control, voltage adjustment and color compensation. Using FACScan and CELLQuest software to analyze the data collected. Using forward scatter side scatter parameter gate. Collect 10000 cells expressed as a percentage of each group. The expression of the cell.
2.2 T lymphocyte proliferation test
2.2.1 human peripheral blood mononuclear cells (PBMC) were extracted: density gradient centrifugation was used to extract peripheral blood samples (PBMC) from severe pneumonia patients and healthy persons.
2.2.2 mononuclear cells (PBMC) staining and culture: PKH26 reference PKH26 dye staining for PBMC instructions. Resuspend into 1 * 106 / ml were inoculated into 24 well culture plate hole. The experiment was divided into 4 groups: blank control group PBS+PKH26 staining after PBMC; the positive control group were stained with PHA+PKH26 PBMC; the thymosin alpha 1+ endotoxin +PKH26 staining after PBMC PKH26+ staining after PBMC.; the endotoxin per hole final volume is about 0.6 ml the concentration of 1 * 106 / ml at 37 DEG C, cultured for 5 days under the condition of 5%CO2.
Detection of 2.2.3 T lymphocyte proliferation after 5 days of culture: remove PKH26 staining cells, divided into two tubes, each tube 0.3ml, centrifugal washing, adding FITC labeled PC5 - CD3 1 g/ 106 cells, mixing at room temperature after dark incubation, after washing, g/L fixed with 2 paraformaldehyde, analysis of T lymphocytes the proliferation index of CELLQuest and ModFitTM software by using flow cytometry and data (PF) precursor frequency and proliferation of cells (PI).
Detection of T lymphocyte 2.2.4 were cultured in vitro and CO molecules: the mononuclear cells were not stained, resuspended into 1 * 106 / mL concentration, were inoculated into 24 well culture plate. The experiment was divided into 4 groups: blank control group PBS+ without PBMC staining; the positive control group PHA+ without the PBMC staining; thymosin alpha 1+ endotoxin + unstained PBMC; the endotoxin + non staining of PBMC. per hole and final volume is about 0.6 ml, the concentration of 1 * 106 / ml at 37 DEG C, cultured for 5 days under the condition of%CO 2. 5 out of unstained cells cultured for 5 days, divided into two tubes, each tube 0.3ml, centrifugal washing. Adding a fluorescein labeled FITC - CD28/PE - CD152/PC5 - CD3 1 g/ 106 cells, mixing at room temperature after dark incubation, after washing, g/L fixed with 2 paraformaldehyde, using flow cytometry and data analysis using CELLQuest software, costimulatory molecules CD28, CD152 expression.
2.3 statistical methods: all data were analyzed by software SPSS 11.5, the measurement data to mean + standard deviation (S) said that the two groups were compared by t test. The random block design data using analysis of variance, multiple comparison between data with LSD method, P0.05 was statistically significant difference.
Result
1 severe pneumonia T lymphocyte subsets and costimulatory molecules: 21 cases of severe pneumonia in patients with CD3, CD4, CD86, HLA-DR, CD28/, CD152, CD4/CD8 compared with 12 cases of healthy control group, there was significant difference (P 0.05); CD8, CD28, CD152 expression increased compared with healthy control group, was statistically significant the difference (P 0.05).
The 228 day survival of patients with severe pneumonia before and after treatment (10 days) of T lymphocyte subsets, and costimulatory molecules: survival group 8 cases of severe pneumonia for tenth days and first days compared with APACHE score decreased significantly (P=0.000); CD28, CD152, CD86, HLA-DR expression was significantly increased (P 0.05); CD3T cells also increased significantly (P=0.030); CD8CD3, CD4CD3 + T cells showed no significant change (P 0.05).
3 PKH26 labeled peripheral blood mononuclear cells (PMBC) in severe pneumonia patients: PKH26 labeled PMBC, and PKH26 fluorescence intensity on the histogram showed a significant right deviation, reaching 104, showing a single peak. The positive rate was 96.48%. after fluorescence microscopy to observe PMBC after PKH26 labeling, and its cells showed red fluorescence.
T lymphocytes in peripheral blood of 4 patients with severe pneumonia on the antigen stimulated proliferation ability: 10 cases of severe pneumonia in patients with peripheral blood T lymphocyte proliferation index (LPS) on endotoxin stimulated PI (1.55 + 0.42) precursor frequency of PF and the proliferation of cells (0.02 + 0.01) is lower than that of 10 healthy people (2.15 of the PI group + 0.29) and PF (0.04 + 0.02), there was significant difference (P 0.05).
Effect of 5 thymosin - alpha 1 on the proliferation of T lymphocyte in peripheral blood of severe pneumonia
Effects of the proliferation of T lymphocytes in peripheral blood of 5.1 optical microscope observation of thymosin alpha 1 on severe pneumonia: T lymphocyte factor group of severe pneumonia in peripheral blood of different intervention after 5 days of culture in vitro, observed by microscope (x 10), visible PHA group and Thymosin alpha 1 plus endotoxin group lymphocyte blastisation obvious the other two groups, no obvious lymphocyte blastogenesis.
On the proliferation of T lymphocytes in peripheral blood of 5.2 of thymosin alpha 1 on severe pneumonia: 10 cases of severe pneumonia in the PHA group, the precursor frequency of thymosin alpha 1 plus endotoxin group and endotoxin group cell proliferation of T cells (PF) were: 0.03 + 0.03,0.03 + 0.02,0.02 + 0.01; T lymphocyte proliferation index (PI) respectively. The proliferation index of cell proliferation and 1.68 + 0.49,1.84 + 0.53,1.55 + 0.42. of thymosin alpha 1 plus endotoxin group T lymphocyte precursor frequency Binet toxin group, a statistically significant difference (P 0.05); compared with the precursor frequency of PHA cells proliferation index and proliferation of thymosin alpha 1 and the toxins of T lymphocytes, there was no statistically significant difference (P 0.05).
Effect of 6 thymosin - alpha 1 on the synergistic stimulator of T lymphocyte in peripheral blood of severe pneumonia
Effect of T CD28 lymphocytes in peripheral blood of 6.1 of thymosin alpha 1 on severe pneumonia and costimulatory molecules: PBS group (67.40 + 6.45)%, group PHA (72.21 + 7.05)%, thymosin alpha 1 plus endotoxin group (73.70 + 8.66)% and endotoxin group (66.94 + 11.85)% of thymosin alpha 1 with CD28 toxin group T lymphocyte costimulatory molecule expression of Binet toxin group and PBS group, there was significant difference (P 0.05); compared with PHA group the expression of thymosin alpha 1 plus endotoxin group T CD28 lymphocyte costimulatory molecules, there was no statistically significant difference (P=0.479).
Effect of T CD152 lymphocytes in peripheral blood of 6.2 of thymosin alpha 1 on severe pneumonia and costimulatory molecules: PBS group (3.01 + 1.08)%, group PHA (2.69 + 1.23)%, thymosin alpha 1 plus endotoxin group (2.41 + 0.77)% and endotoxin group (2.86 + 1.03)% of thymosin alpha 1 internal toxin group T lymph cell CD152 costimulatory molecule expression Binet toxin group and PBS group, there was significant difference (P 0.05); compared with PHA group the expression of thymosin alpha 1 plus endotoxin group T CD152 lymphocyte costimulatory molecules, there was no statistically significant difference (P=0.306).
Co stimulation T lymphocytes in peripheral blood of 6.3 of thymosin alpha 1 on severe pneumonia and effect of molecular ratio of CD28/CD152: PBS group (25.26 + 9.57), PHA group (31.38 + 11.67), thymosin alpha 1 plus endotoxin group (33.30 + 9.96) and endotoxin group (21.13 + 5.39) - alpha thymosin plus 1 LPS. In group of T lymphocytes and the ratio of CD28/CD152 Binet toxin group and PBS group, there was significant difference (P 0.05); thymosin alpha 1 plus endotoxin group T lymphocyte costimulatory molecules compared with PHA group the ratio of CD28/CD152, no statistically significant difference (P=0.490).
conclusion
1. the T lymphocyte in peripheral blood of patients with severe pneumonia has "immune inability", which leads to the decrease of T lymphocyte and CD4 subgroup, which inhibits the immune function of the body.
The abnormal expression of 2. T lymphocyte related co stimulators, CD28, CD152 and CD86, is involved in the pathophysiological process of severe pneumonia.
3. in vitro thymosin alpha 1 can improve the proliferation of T lymphocytes in patients with severe pneumonia by improving the expression of CO stimulatory molecules CD28 and CD152 in severe pneumonia patients.

【學(xué)位授予單位】：廣州醫(yī)學(xué)院
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2009
【分類號(hào)】：R392

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