不同分离方法对小鼠脾脏调节性T细胞表达特征的影响

近年来,随着以变应性鼻炎（AR）和变应性哮喘为代表的呼吸道变应性疾病在全球范围内发病率的升高,与之发病机制密切相关的CD4＋CD25＋T细胞及其特异性标志物Foxp3成为近年来的研究热点。在此前的实验中,我们对AR小鼠外周调节性T细胞（regulatory T cell,Treg）的表达特征进行了研究,发现实验组与正常对照组外周血表达有显著性差异,而脾脏表达两组间无显著性差异[1]。     

过氧化物酶体增殖物激活受体γ激动剂对小鼠变应性鼻炎治疗的作用与机制研究

目的　探讨过氧化物酶体增殖物激活受体（peroxisome proliferators-actived receptor,PPAR）γ激动剂对小鼠变应性鼻炎的治疗作用及机制。方法　采用卵清蛋白（OVA）建立变应性鼻炎小鼠模型,观察吡格列酮（PIO）对变应性鼻炎症状的改善;取鼻腔组织行HE染色,采用real time PCR检测脾脏Foxp3、T-bet、GATA-3 mRNA表达;流式细胞仪检测脾脏中CD4+Foxp3+T细胞含量。结果　小鼠变应性鼻炎组（AR组）喷嚏和搔鼻频率明显高于对照组（control组）,经PIO治疗后症状得以改善;AR组小鼠鼻黏膜上皮连续性破坏,黏膜下大量炎症细胞浸润;PIO治疗后炎症细胞浸润明显减少,同时上皮完整性修复良好;PIO组Foxp3 mRNA表达高于AR组（P <0.001）,GATA-3则较AR组明显降低（P <0.001）,而T-bet 无统计学差异;AR组CD4+Foxp3+T细胞含量（4.43%±0.25%）较control组（5.19%±0.39%）降低（P <0.001）,PIO治疗后CD4+Foxp3+T细胞含量（6.35%±0.37%）高于control组及AR组。结论　PPARγ激动剂能够有效缓解小鼠鼻过敏症状,调节Th1/Th2平衡;PPARγ激动剂可能是通过促进Foxp3表达,进而扩增调节性T细胞达到治疗变应性鼻炎的作用。     

流式细胞术检测IFN-γ、IL-4在鼻息肉及变应性鼻炎患者外周血表达的差异

目的检测鼻息肉及变应性鼻炎患者外周血单个核细胞（PBMC）内IL-4，IFN-γ的表达，探讨细胞因子与鼻息肉和变应性鼻炎发病的关系，以及二者发病机制的不同。方法用流式细胞仪测定30例鼻息肉患者、30例变应性鼻炎患者和30例健康人的PBMC，经PMA诱导培养后IFN-γ／和IL-4的水平，与健康对照组比较，进行统计学分析。结果鼻息肉组PBMC中CD3^＋／CD8^-／IFN-γ^＋和CD3^＋／CD8^-／IL-4^＋含量均较健康对照组明显升高，比较有统计学意义（P〈0．05）。变应性鼻炎组PBMC中CD3^＋／CD8^-／IFN—γ^＋含量较健康对照组明显降低，而CD3^＋／CD8^-／IL-4^＋含量则明显升高，比较均有统计学意义（P〈0．05）。结论鼻息肉患者体内分泌IFN-γ、IL-4均增高，分泌多种细胞因子，在鼻息肉的发生发展中起到网络调节作用。而变应性鼻炎患者分泌IL-4增高，分泌IFN-γ却受到抑制，这种细胞因子失平衡可能在变应性鼻炎发病机制中起到重要作用。     

鼻炎冲剂治疗变应性鼻炎的免疫调节机制探讨

目的 探讨鼻炎冲剂治疗变应性鼻炎的免疫调节机制.方法 选择30例常年性变应性鼻炎患者,予鼻炎冲剂连续口服2月,进行疗效评估;采用流式细胞仪测定20例正常对照组及30例患者组治疗前后外周血单个核细胞的CD4+CD25+Foxp3+T细胞占CD4+CD25+T细胞比例;同时采用ELISA法测定血清IL-10、IFN-γ的含量.结果 治疗组有效率为86.7％;外周血单个核细胞中CD4+CD25+Foxp3+T细胞占CD4+CD25+T细胞比例:治疗组治疗前16.83±2.94％,治疗后19.38±3.71％;对照组20.75±4.64％.血清IL-10含量(pg/ml):治疗组治疗前6.87±1.08,治疗后11.97±1.62;对照组13.18±1.56.血清IFN-γ含量(pg/ml):治疗组治疗前14.77±2.13,治疗后14.56±2.29;对照组15.65±1.93.结论 本研究提示鼻炎冲剂可通过提高外周血单个核细胞中CD4+CD25+Foxp3+T细胞数量及血清IL-10含量有效治疗变应性鼻炎.     

变应性鼻炎患者血清维生素D与Treg/Th17细胞的相关性研究

目的　通过检测变应性鼻炎（AR）患者血清中维生素D（vitamin D,VD）及外周血调节性T细胞（regulatory T cell,Treg）、Th17细胞的表达水平,研究Treg细胞、Th17细胞及VD在AR发病机制中的作用,探讨VD与Treg/Th17细胞间的相互关系以及治疗AR的价值。方法  选取38例AR确诊患者为AR组,健康体检者38例为对照组。采用酶联免疫吸附试验（ELISA）检测受试者外周血25（OH）D3的含量;电化学发光免疫分析法检测血清总VD含量;流式细胞术（FCM）检测外周血CD4+IL-17+Th17细胞、CD4+CD25+Foxp3+Treg细胞占CD4+T细胞百分率。结果　AR组血清总VD及25（OH）D3的表达水平显著低于对照组（t =-7.791、-2.439,P 均<0.05）;AR组CD4+CD25+Foxp3+Treg细胞占CD4+T细胞的百分率明显低于对照组（t =-17.011,P <0.05）;AR组CD4+IL-17+Th17细胞占CD4+T细胞的百分率明显高于对照组（t =8.986,P <0.05）;AR组外周血CD4+CD25+Foxp3+Treg细胞表达水平与血清25（OH）D3含量呈正相关（r =0.713,P <0.05）;AR组外周血CD4+IL-17+Th17细胞含量与血清25（OH）D3含量呈负相关（r =-0.658,P <0.05）。结论　AR患者中VD含量显著低于对照组,提示血清VD的缺乏有可能影响AR发病;而VD缺乏可能与Treg/Th17细胞失衡存在一定的相关性。     

变应性鼻炎患者外周血Th1和Th2细胞的流式细胞分析

体内Th1和Th2细胞及其分泌的细胞因子失平衡在变应性鼻炎的发病机制中所起的作用受到学者们的重视。通过检测变应性鼻炎患者外周血单个核细胞（PBMC）经PMA刺激培养后的CD3^＋／CD8^-细胞的IL-4和IFN-γ的水平，进一步探讨Th1／Th2失衡在变应性鼻炎发病中所起的作用。     

小鼠脾脏调节性T细胞分离纯化方法比较

在变应性鼻炎的基础研究中,探讨调节性T细胞（T regulatory cell,Treg细胞）中转录因子FoxP3对细胞因子受体Ebi3表达调控的分子机制,是以小鼠脾脏淋巴细胞为研究对象,可以通过CD荧光抗体标记,免疫磁珠分选法或流式细胞分选法获得Treg细胞。因此,建立有效的小鼠脾脏淋巴细胞分离技术是至关重要的前期工作,是进行这些研究的先决条件。本文采用了两种方法对小鼠脾脏Treg细胞进行分离,并对脾脏Treg细胞活性与获得率进行了比对分析。     

螨变应原特异性免疫治疗1年后免疫学变化

目的探讨标准化尘螨变应原疫苗进行集群免疫治疗过程中的免疫学机制。方法将60例螨过敏变应性鼻炎（AR）患者分为集群免疫治疗组（n=30）和药物治疗组（n=30）。检测基线和治疗1年后受试者血清中总IgE、螨特异性IgE、特异性IgG4水平,通过流式细胞术检测外周血单核细胞中Th1、Th2、天然调节性T细胞（CD4^＋CD25^＋Foxp3^＋ T细胞）和I型调节性T细胞（Tr1细胞,CD4^＋IL-10^＋IL-4^-T细胞）在CD4^＋T细胞中百分比。结果经过1年治疗后,总IgE和螨特异性IgE水平未见明显改变,但免疫治疗组患者血清中螨特异性IgG4水平明显升高（P〈0．0001）。Th1、Th2型细胞和天然调节性T细胞（CD4^＋CD25^＋Foxp3^＋T细胞）占CD4^＋T细胞的百分比在治疗前后均无明显变化（P=ns）,而Tr1细胞在免疫治疗1年后明显增高（P〈0．001）。结论特异性IgG4和Tr1细胞增高可作为产生免疫耐受的免疫学指标。     

齐墩果酸通过抑制自噬调节变应性鼻炎中的Treg/Th17细胞失衡CSCD

目的探讨齐墩果酸对变应性鼻炎(AR)中调节性T细胞(regulatory T cells,Treg)/辅助性T细胞17(helper T cells 17,Th17)的调节作用及潜在机制。方法收集AR患者鼻黏膜组织及外周血单个核细胞(peripheral blood mononuclear cell,PBMC)。饲养BALB/c小鼠。PBMC用于建立AR细胞模型,BALB/c小鼠用于建立AR动物模型。对于AR细胞使用150μg/ml的齐墩果酸进行治疗。对于AR小鼠使用低剂量(L)-齐墩果酸(50 mg/kg)、高剂量(H)-齐墩果酸(200 mg/kg)、自噬抑制剂3-MA(10 mg/kg)、H-齐墩果酸+自噬激活剂雷帕霉素(Rapa,1 mg/kg)分别进行治疗。qRT-PCR测人鼻黏膜组织IL-17A和Foxp3的表达以及小鼠各组鼻黏膜组织中RORγt和Foxp3的表达。流式细胞术从PBMC中分选Th17和Treg细胞,并检测PBMC中白细胞介素17A(IL-17A)细胞和叉头样转录因子3(Foxp3)细胞的比例。Western blot法检测Th17和Treg细胞中自噬相关蛋白Beclin1、LC3-II、LC3-I、p62的表达。酶联免疫吸附试验检测各组小鼠鼻腔灌洗液中IL-17A和IL-10的表达。结果AR组患者鼻黏膜组织中IL-17A表达显著增加,但Foxp3的表达显著降低(P均<0.05)。齐墩果酸下调PBMC中IL-17A的表达,并上调Foxp3的表达。齐墩果酸抑制Th17细胞和Treg细胞中Beclin1、LC3-II以及LC3-I的表达(P均<0.05),促进p62的表达水平。齐墩果酸降低AR小鼠体内IL-17A和RORγt水平,并上调IL-10和Foxp3的水平(P均<0.05)。结论齐墩果酸通过抑制自噬信号改善AR中Th17/Treg细胞的平衡。     

调节性T细胞与IgE、IL-4、IL-5在变应性鼻炎小鼠和鼻用激素抗炎中的实验研究

目的 探讨CD4+CD25+FOXP3+调节性T细胞(regulatory T cells, Tregs)与IgE、IL-4、IL-5在变应性鼻炎(allergic rhinitis, AR)小鼠及鼻用激素抗炎中的表达及作用。方法 5～6周龄雌性Balb/c小鼠30只,随机分为正常组、AR组和鼻用激素组。正常组无干预;AR组采用卵清蛋白(ovalbumin,OVA)全身致敏并雾化和滴鼻激发;鼻用激素组在成功致敏后,每次激发完30min后雾化吸入丙酸氟替卡松10min。小鼠于末次激发24h后处死,鼻黏膜行苏木素-伊红染色;流式检测气管旁引流淋巴结和脾脏中CD4+CD25+FOXP3+Tregs表达; ELISA检测血清中OVA 特异性IgE及鼻腔灌洗液中IL-4、IL-5含量。结果 与正常组小鼠相比,AR组小鼠鼻黏膜出现大量的嗜酸性粒细胞(EOS),CD4+CD25+FOXP3+Tregs表达在气管旁引流淋巴结中上调,脾脏中无差别;IgE、IL-4、IL-5含量明显升高,而鼻用激素组小鼠CD4+CD25+FOXP3+Tregs在气管旁引流淋巴结和脾脏中表达继续明显上调;EOS数目与IgE、 IL-4、IL-5含量均被明显抑制。结论 CD4+CD25+FOXP3+Tregs不仅在AR中,而且在鼻用激素对AR的干预中都发挥着重要的免疫调节作用,同时IgE、IL-4、IL-5介导变应性炎症反应,在AR的发生发展中发挥重要作用。     

儿童分泌性中耳炎耳积液中免疫相关指标表达分析

目的 探讨儿童分泌性中耳炎患者中耳积液中的免疫相关指标变化情况。 方法 选取2016年12月至2017年12月收治的30例分泌性中耳炎患儿设为研究组,选取同期体检的健康儿童30例设为对照组。比较两组外周血中CD4⁺T、CD8⁺T细胞百分数及CD4⁺ /CD8⁺比值。比较研究组中耳积液及血浆中IL-2、IL-4、IL-6水平。将研究组外周血CD4⁺,CD8⁺T细胞值与中耳积液中IL-2、IL-4、IL-6值进行相关性分析。 结果 研究组外周血中CD4⁺T、CD8⁺T细胞百分数均明显高于对照组,CD4⁺ /CD8⁺比值明显低于对照组,差异有统计学意义(P<0.01)。研究组中耳积液中IL-2、IL-4、IL-6水平均明显高于血浆,差异有统计学意义(P<0.01)。研究组血浆中IL-2、IL-4、IL-6水平均明显高于对照组,差异有统计学意义(P<0.01)。Pearson直线相关分析结果显示,研究组中耳积液中IL-2、IL-4、IL-6水平与外周血CD4⁺T、CD8⁺T含量均呈显著正相关(P<0.01)。 结论 分泌性中耳炎与强烈的免疫反应密切相关,存在CD4⁺T、CD8⁺T细胞亚群显著升高的现象,IL-2、IL-4、IL-6对于儿童分泌性中耳炎的诊断具有一定的临床意义。     

Persistent inflammation and hyperresponsiveness following viral rhinosinusitis

OBJECTIVES: To develop a murine model of viral rhinosinusitis. STUDY DESIGN: Randomized, controlled, animal model. METHODS: Mice were intranasally inoculated with Sendai virus (SeV) or ultraviolet (UV)-inactivated virus. On days 3 and 10 postinfection, nasal lavage fluid was obtained for viral culture. On days 4, 10, and 38 postinfection, sinus mucosa was harvested and analyzed by flow cytometry for CD3-, CD4-, CD8-, CD25-, CD11b-, CCR3-, and GR1-positive cells. Nasal hyperresponsiveness to histamine challenge was measured on days 8 and 36 postinoculation. RESULTS: On day 3, viral cultures were positive from all SeV-inoculated mice but from none of the UV-inactivated mice (P相似文献   

共刺激分子OX40/OX40L在小鼠变应性鼻炎发病机制中的作用

目的 探讨OX40/OX40L在小鼠变应性鼻炎发病机制中的可能作用。方法 精选30只清洁级小白鼠,随机分成对照组、模型组、干预组。通过免疫组织化学方法测定对照组和模型组小鼠鼻黏膜中OX40的表达,同时应用ILISA法测定各组中IL-4、IL-10、IFN -γ的水平。结果 OX40在变应性鼻炎小鼠鼻黏膜上皮细胞、腺体细胞、血管内皮细胞、CD4+T细胞中均呈现高表达,OX40主要表达于细胞膜、细胞浆,在对照组中极少表达（P<0.05）。ILISA法测定IL-4、IL-10、IFN -γ在对照组与模型组间差异有统计学意义（P<0.05）,模型组和干预组相比差异有统计学意义（P<0.05）。结论 OX40/OX40L在变应性鼻炎小鼠发病机制中起重要作用。     

Cure of an established nonimmunogenic tumor,SCC VII,with a novel interleukin 12-based immunotherapy regimen in C3H mice

OBJECTIVE: To develop a murine model of effective treatment with immunotherapy for established head and neck squamous cell carcinoma. DESIGN: Prospective animal study.Subjects Female C3H mice, 8 to 12 weeks old. INTERVENTIONS: A subcutaneous inoculation of 2 x 10(5) SCC VII cells in C3H mice was established for 7 to 12 days. Tests for concomitant immunity were performed, with and without interleukin 12 modification. Tumors were also tested for responsiveness to interleukin 12 (5 mice) and to cyclophosphamide followed by interleukin 12 (5 mice). SCC VII tumors in 24 mice were treated with interleukin 12 followed by cyclophosphamide and interleukin 12. Five mice with tumors treated with isotonic sodium chloride solution served as controls. Tumors were measured 3 to 4 times weekly, and cure was defined as complete regression of the tumor for at least 60 days. Cured mice were rechallenged with 2 x 10(5) SCC VII cells to verify antitumor immunity. Immunohistochemistry of regressing tumors was performed for CD4+ and CD8+ T cells. RESULTS: Tumor-bearing mice easily developed second tumors when challenged with 2 x 10(5) tumor cells in the opposite flank. However, interleukin 12 treatment provided immunity to second tumors in 8 (100%) of 8 mice when started at day 4 and in 2 (40%) of 5 when treated from day 7. SCC VII did not respond to standard interleukin 12 or cyclophosphamide plus interleukin 12 therapy. Seventy-five percent of animals (18/24) treated with interleukin 12 followed by cyclophosphamide plus interleukin 12 were successfully cured, and all cured mice resisted subsequent challenge with SCC VII. Immunohistochemistry of regressed tumors showed an intense CD4+ and CD8+ infiltrate that was absent in the untreated and nonresponding tumors. CONCLUSIONS: Nonimmunogenic SCC VII is a nonimmunogenic tumor that can be converted into an immunogenic tumor with interleukin 12 treatment. Additional treatment with cyclophosphamide plus interleukin 12 leads to complete regression in 75% of mice.     

小儿咽喉炎使用复方芩兰口服液的治疗效果研究

目的探讨小儿咽喉炎采用复方芩兰口服液治疗的临床疗效。方法选取2019年10月至2020年12月在我院治疗的小儿咽喉炎68例作为研究对象,按照治疗方法的不同分成观察组和对照组各34例,对照组采用磷酸奥司他韦颗粒治疗,观察组采用复方芩兰口服液,比较两组患儿临床疗效、临床症状消失时间、免疫功能指标、炎性因子水平的影响情况。结果在临床疗效上,观察组明显高于对照组(P<0.05);在临床症状消失时间上,观察组明显短于对照组(P<0.05);在免疫功能指标方面,两组治疗后CD3⁺、CD4⁺较治疗前均有明显上升(P<0.05),治疗后CD8+均明显下降(P<0.05),观察组治疗后CD3⁺、CD4⁺明显高于对照组(P<0.05),CD8+明显低于对照组(P<0.05);在炎性因子水平上,两组治疗后较治疗前均有明显下降(P<0.05),观察组治疗后明显低于对照组(P<0.05)结论小儿咽喉炎采用复方芩兰口服液治方式有明显效果,能够改善患儿的临床症状,提高免疫功能,减少炎症反应,值得临床推广。     

Human nasal polyp microenvironment maintained in viable and functional states as xenografts in SCID mice

OBJECTIVES: We undertook to maintain human nasal polyp tissue in a viable and functional state in SCID (severe combined immunodeficiency) mice. METHODS: Small, nondisrupted pieces of human nasal polyp tissues were subcutaneously implanted into SCID mice depleted of natural killer cells. The resulting xenografts were examined histologically, and the sera were evaluated for the presence of human protein. RESULTS: The original histologic architecture of the polyp was maintained in the xenografts. The tissues, including pseudostratified columnar epithelial-lined polyps and subepithelial stroma, remained viable, and goblet cells continued to produce mucin for up to 26 weeks after engraftment. Human inflammatory leukocytes, including CD3+ T cells, CD20+ B cells, CD138+ plasma cells, and CD68+ monocytes and/or macrophages, were present. Identification of human immunoglobulin and human interferon-gamma in the sera of xenograft-bearing mice indicated that the B cells or plasma cells and T cells within the xenografts remained functional for 2 weeks after engraftment. CONCLUSIONS: The ability to engraft and maintain nasal polyps provides an in vivo human/mouse chimeric model with which to investigate the role of inflammatory leukocytes and stromal cells in the maintenance and progression of polyposis and to determine how exogenous cytokines may alter the interaction of inflammatory cells, stromal cells, and epithelial cells in the polyp.     

Pathogenic role of tonsillar lymphocytes in associated with HSP60/65 in Pustulosis Palmaris et Plantaris

Objective

We aimed to define role of tonsillar lymphocytes (TL) and immune cross-reactivity between bacterial-HSP65 and human-HSP60 in Pustulosis palmaris et plantaris (PPP), an intractable chronic disease characterized with pustules and cornification of palms and soles.

Methods

Two sets of crossover trials were designed by employing SCID mice model. In the first trial, mice were transplanted with tonsillar lymphocytes and skin-grafts from PPP patients (TL group). In the second trial, mice were transplanted with tonsillar lymphocytes from PPP patients and injected with recombinant human HSP60. Control groups were designed for each step. Comparisons were performed for immunologic analyses including infiltration of CD4+ lymphocytes in skin-grafts by immunostaining, and levels of anti-HSP65-IgG and cytokines in mice sera by enzyme-linked immunosorbent assay (ELISA).

Results

In TL group, infiltration of CD4+ lymphocytes in skin-grafts were significantly higher than mice transplanted with blood lymphocytes (p < 0.05), while anti-HSP65-IgG levels in sera showed non-significant tendency to increase in the TL group. CD4+ cells and anti-HSP65-IgG levels were also well-correlated with each other in TL group (p < 0.01). Besides, anti-HSP65-IgG levels were significantly correlated with cytokine levels (IL-6, IFN-γ) in mice sera (p < 0.01). We found strong expression of HSP60 in PPP lesions. Finally, HSP60-stimulation in mice transplanted with TL from PPP patients induced significantly higher anti-HSP65-IgG levels in serum compared to control groups including mice without HSP60-stimulation or peripheral blood lymphocytes-transplanted mice or transplanted with TL from control patients (p < 0.05).

Conclusion

Our results indicate the pathogenic role of TL and immune cross-reaction between human-HSP60 and bacterial-HSP65 in PPP.     

Signals through CD40 play a critical role in the pathophysiology of Schistosoma mansoni egg antigen--induced allergic rhinitis in mice

BACKGROUND: Interaction between CD40 and CD40L is thought to regulate immune responses in several allergic diseases. However, little is known about its in vivo role in the pathophysiology of allergic rhinitis. We sought to determine whether the lack of signals through CD40 affects the pathophysiology of allergic rhinitis using a murine model. METHODS: Wild type (WT) and CD40-deficient BALB/c (CD40-/-) mice were sensitized intranasally to Schistosoma mansoni egg antigen (SEA). After repeated sensitization, histamine responsiveness, serum antibody titer including immunoglobulin E (IgE), nasal eosinophilia, and cytokine production by nasal mononuclear cells were determined in each group. RESULTS: Intranasal sensitization with SEA in WT mice elicited a strong Th2 response including SEA-specific IgE production, nasal eosinophilia, and interleukin (IL)-4, and IL-5 production by nasal mononuclear cells after antigen challenge. Production of SEA-specific IgE and IgG1 was abolished in SEA-sensitized CD40-/- mice. These mice showed impaired nasal eosinophilia and displayed markedly reduced histamine-induced nasal hyperresponsiveness as compared with WT mice. Furthermore, reduced production of IL-4 and IL-5 by nasal mononuclear cells was seen in CD40-/- mice. CONCLUSION: These results show that signals through CD40 play a critical role in not only IgE production but also pathophysiology of allergic rhinitis such as nasal hyperresponsiveness and nasal eosinophilia.     

Localization of T cells and subtypes in the paranasal sinus and turbinate mucosa in patients with chronic sinusitis

The aim of this study was to quantitate total T lymphocytes (total CD3+ cells) and T-lymphocyte subtypes (CD4+ [T helper] and CD8+ [T suppressor] cells) in patients with chronic sinusitis who were treated with functional endoscopic sinus surgery (FESS) and to investigate the pathophysiology of persistent inflammation in chronic sinusitis. This prospective study was conducted in study and control groups. The study group consisted of 32 patients (20 male, 12 female) with chronic sinusitis who underwent FESS. The control group consisted of 8 nonsinusitis patients (5 male, 3 female) who underwent septoplasty. Specimens from the study group were excised from five regions: the uncinate process, maxillary and ethmoid sinuses, and middle and inferior turbinates. The specimens were examined with x10 magnification by light microscopy, and the slides with a severe inflammatory process were included. Punch biopsy of the control group was taken from the inferior turbinate with patients' written approval. The surgical specimens from the study and control groups were examined with an immunohistochemical staining technique with monoclonal antibodies against CD3, CD4, and CD8 surface antigens of T lymphocytes. In every specimen, the numbers of CD3+, CD4+, and CD8+ cells were calculated in 3 to 4 high magnification field on light microscopy, and the mean number of these cells in the epithelium, subepithelial layer of the lamina propria, and deep paraglandular layer of the mucosa was determined. Statistical analysis by Kruskal-Wallis analysis of variance and the Mann-Whitney U test with Bonferroni correction revealed that the CD3 epithelial layer value of the inferior turbinate (p = .030) and the CD4 deep layer value of the middle turbinate (p = .048) were significantly higher than the corresponding values of the control group. In the epithelial (p = .018) and subepithelial (p = .012) layers of the uncinate process group, in the epithelial (p = .050) and subepithelial (p = .012) layers of the ethmoid sinus group, and in the subepithelial (p = .018) and deep paraglandular (p = .012) layers of the middle turbinate group, the difference between the CD4+ and CD8+ cell counts was found to be statistically significant by the Wilcoxon signed rank test. The number of CD4+ cells was higher than the number of CD8+ cells. In conclusion, T cells play a role in the pathophysiology of chronic sinusitis. CD4+ T helper cells, in particular, are predominant at the initiation and regulation of inflammation. The uncinate process, ethmoid sinus, and middle and inferior turbinates have the main roles by T cells and subtypes in the defense system in chronic sinusitis.