结节病肉芽肿病变中有螺旋体吗

目的观察结节病肉芽肿病变内有无螺旋体,进一步探讨结节病螺旋体致病的可能性。方法收集50例结节病病理检查标本,活检47例,尸检3例,对其石蜡包埋组织进行连续切片,用HE染色观察组织病理学形态,用W arth in-Starry(W-S)银染色、免疫组化染色及透射电镜观察寻找螺旋体。螺旋体染色及观察的阳性对照为伯氏包柔疏螺旋体(Borrelia burgdorferi,BB)菌株的涂片及培养标本和5例Ⅱ期梅毒的活检标本。结果在结节病肉芽肿病变内未发现螺旋体。结论本研究未能就结节病的螺旋体感染假说提供直接的病原学证据。     

结节病肉芽肿细胞内空气细颗粒物元素组成及来源分析

目的 分析结节病肉芽肿细胞(吞噬细胞、类上皮细胞、多核巨细胞)内空气细颗粒物(PM2.5)的元素组成及来源,探讨结节病与PM2.5的相关性.方法 收集50例结节病病变组织、10例非结节病成人尸检肺组织、18例PM2.5支气管灌注染毒大鼠肺组织(有肉芽肿病灶)石蜡包埋标本,采集大气中PM2.5,分别行HE染色、沃森-斯塔理(Warthin-Starry,WS)银染色,应用共聚焦显微镜拉曼光谱和透射电镜-能谱对上述部分病例标本肉芽肿细胞和尘细胞内的PM2.5及大气PM2.5的成分进行分析,用X线荧光分析技术对所采集大气PM2.5的主要元素成分进行分析.结果 结节病病变组织、非结节病成人尸检肺组织、PM2.5支气管灌注染毒大鼠肺组织及大气中PM2.5共4组标本中PM2.5的拉曼光谱和元素组成非常相似,均以碳质成分为主要特征.结论 为结节病肉芽肿细胞中的PM2.5来源于大气PM2.5提供了进一步的依据,从而不能完全除外结节病患者可能是对PM2.5易感的个体的可能性.

Abstract：

Objective To explore the source of the fine particulate matter (PM2.5) in the sarcoidosis granulomatous cell and the relationship between the sarcoidosis and the PM2.5 in the atmosphere.Methods Paraffin-embedded tissues of 50 cases of human sarcoidosis biopsy samples, 10 cases of nonsarcoidosis autopsy lung samples, 18 cases of lung tissues (with granulomatous lesions) of rats exposed to PM2.5 by bronchial infusion, and the free PM2.5 sample in the atmosphere were collected. The characteristics of tissues above mentioned were observed under the light microscopy, which stained by HE staining and Warthin-Starry silver staining. The characteristics of the PM2.5 in the four groups were analyzed using confocal Raman microscopy. The component of the PM2.5 in the sarcoidosis granuloma was analyzed using transmission electron microscope-energy dispersive X-ray detector (TEM-EDX), and the component of the PM2.5 in the atmosphere was analyzed with X-ray fluorescence separately. Results The PM2.5 in the four groups have the similar Raman spectrum, they share the feature of carbonaceous composition, the element component of PM2.5 in the human sarcoidosis was the same as PM2.5 in the atmosphere. Conclusion The study provided the further evidence that the PM2.5 in the sarcoidosis lesion was from PM2.5 in the atmosphere,and it should be not excepted that sarcoidosis may be a sensitive individual reaction to the PM2.5 inhaled from the atmosphere.     

羊水栓塞的病理诊断

目的探讨羊水栓塞病人病理诊断的有关问题。方法通过HE染色、胆色素和黏液组织化学染色以及CD34、cytokeratin(H)、HCG-β免疫组化染色，对死于围产期的13例尸检资料及1例抢救成功的外检资料进行回顾性分析。结果尸检中明确诊断为羊水栓塞的5例，在其HE染色的肺组织切片中小血管及毛细血管内都看到了长梭形，三五成团或散在分布的鳞状上皮，其中4例观察到胎粪小体的存在，经胆色素染色证实，3例观察到黏液，2例经黏液染色证实。1例外检诊断为羊水栓塞抢救成功的病例在子宫小血管及毛细血管内也看到了鳞状上皮，并经免疫组化标记证实。其他8例病例，无1例观察到明确羊水成分，其中6例在肺小血管内发现红染、丝状细胞团，但量少且无其他羊水成分证据，cytokeratin(H)全部阴性，CD34染色有3例阳性，3例在肺血管或子宫血管内看到了大细胞，HCG染色均为阴性。结论羊水栓塞的病理诊断应该以HE切片结合病史及临床表现为主，特殊染色及免疫组化染色可以辅助诊断，但不应完全依赖于特殊染色及免疫组化染色。     

严重急性呼吸综合征患者尸解肺标本的病理改变和致病机制研究

目的研究严重急性呼吸综合征（SARS）患者尸解肺标本的病理改变和致病机制。方法观察了2003年4-7月期间死于SARS的6例患者的肺标本,并采用光镜、电镜、Masson三色染色和免疫组织化学染色方法（EnVision法）进行研究。结果肺标本的病理形态改变：（1）6例的双肺均可见到弥漫性实变病灶,肺重量明显增加;（2）6例均可见到弥漫性肺泡损伤,包括透明膜形成、肺泡腔内水肿／出血、纤维素沉积和肺泡上皮细胞脱屑,AE1／AE3免疫组织化学染色显示肺泡上皮细胞的完整性明显破坏;（3）Ⅱ型肺泡上皮细胞轻度增生,有一定异型性,细胞体积增大,胞质呈双染性和颗粒状,胞质内可见小脂肪空泡聚集（5／6）;（4）6例中有5例可见巨细胞在肺泡内浸润,巨细胞大多AEl／AE3阳性（5／6）,少数CD68阳性（2／6）;（5）组织学形态和免疫组织化学染色证实肺泡腔内和肺泡间隔内有多量巨噬细胞浸润（6／6）;（6）6例中有5例可见巨噬细胞噬红细胞象;（7）6例中有5例可见肺纤维化,包括肺泡间隔和肺间质增宽（5／6）、肺泡腔内渗出物机化（6／6）和胸膜增厚（4／6）。Masson三色染色证实胶原纤维明显增生,免疫组织化学染色显示大多数为Ⅲ型胶原。光镜和免疫组织化学染色显示5例有明显的成纤维细胞／肌纤维母细胞增生灶;（8）5例可见支气管黏膜鳞状上皮化生;（9）6例患者均可见血栓;（10）2例同时合并其他感染,1例合并细菌感染,另1例合并真菌感染。此外,电镜发现在肺泡上皮细胞和肺血管内皮细胞的胞质内有冠状病毒样颗粒。结论SARS冠状病毒直接损伤肺泡上皮细胞、巨噬细胞明显浸润和成纤维细胞／肌纤维母细胞显著增生在SARS的致病机制中起重要作用。     

血管树突状细胞在人主动脉粥样硬化早期病变中的分布

目的：探讨血管树突状细胞在人早期动脉粥样硬化(AS)病变中的分布模式。方法：人主动脉标本15例主要取自尸检和外科手术，常规连续切片，分别行HE及S100／CD1a免疫细胞化学染色，光镜下观察S100／CD1a阳性细胞分布情况。结果：15例HE染色标本中，2例正常，13例人动脉血管可见内膜的增厚及泡沫细胞等AS早期病理表现。9例S100／CD1a染色阳性，阳性率为69．2％。S100／CD1a阳性细胞分布在病变的内膜和外膜，外膜的S100／CD1a阳性细胞主要分布在滋养血管的周围。结论：在AS早期病变部位有血管树突状细胞的聚集，主要分布在病变血管的内膜和外膜，提示血管树突状细胞可能参与了AS早期的免疫反应。     

肺上皮—肌上皮肿瘤一例及其组织发生学研究

肌上皮瘤生要发生在腮腺、颌下腺、胯、颊、牙龈、磨牙后区、口底部、鼻咽及乳腺《包括男性乳腺），发生于支气管和肺较罕见。本文从胚胎发生学角度探讨肺上皮一肌上皮瘤的组织发生，并对其组织结构、细胞形态和诊断标准进行讨论。一、材料、方法和临床资料收集本教研室的外科手术切除、尸检、妇产科引产胎儿的肺标本共27例。其中：（1）胎儿肺20例（胎龄3个月：3例；4个月：3例；5个月：3例；6个月：4例；7个月：2例；8个月；1例；9个月：4例）；（2）新生儿尸检肺：3例；（3）成人尸检肺：3例；（4）肺上皮一肌上皮瘤1例。（1）～（3）三…     

移植骨髓间充质干细胞减轻脂多糖诱导的小鼠急性肺损伤

目的 观察移植骨髓间充质干细胞 （MSCs） 对脂多糖 （LPS） 诱导小鼠急性肺损伤 （ALI）的治疗修复作用。方法 全骨髓培养法培养小鼠骨髓MSCs;细胞免疫化学染色鉴定MSCs特异表面标记;小鼠咽后壁吸入LPS制造小鼠肺损伤;尾静脉注射引入MSCs;称重计算肺水肿指数;肺组织切片HE染色观察组织病理改变;ELISA检测肺泡灌洗液和肺组织匀浆中IL-1β含量;Brdu（5-Bromo-2-Deoxyuridine）标记供体MSCs,免疫组织化学染色及双染色观察移植细胞的迁移和分化状态。结果 培养的MSCs细胞表面标记CD44阳性,而造血系表面标记CD34阴性。吸入LPS后,小鼠出现典型的肺损伤病理改变,肺水肿指数和肺组织匀浆IL-1β含量明显增加。标记的MSCs移植入同种异体的肺损伤小鼠,其肺部出现标记的MSCs,并表达上皮细胞标志抗原-细胞角蛋白（CK）。治疗后小鼠的肺水肿指数和肺组织匀浆IL-1β含量下降。结论 外源性MSCs移植到肺损伤小鼠体内,可迁移至肺损伤部位,并表达上皮细胞标志;减轻肺水肿程度,减少炎症因子释放。     

猫抓病性淋巴结炎的临床病理分析

目的：探讨猫抓病性淋巴结炎的诊断和鉴别诊断要点,方法：应用免疫组化S－P法对26例猫抓病性淋巴结炎分别标记CD20、CD3、CD68;15例进行Warthin-Starry银染色,结果：早期微脓生肉芽肿21例,其病变特征是微脓肿和肉芽肿形成。淋巴结早期微脓肿周围为CD20＋的B淋巴细胞和CD68＋组织细胞,当典型微脓肿性肉芽肿形成时,CD68＋的类皮细胞呈放射状排列,其间夹有CD3＋T淋巴细胞;15例中12例Warthin-Starry染色（＋）。结论：猫抓病灶性淋巴结炎的主要特征是微脓肿性肉芽肿形成,免疫组化标记有助于识别病变中反应增生的细胞成分,本病可能与细菌感染所诱导的细胞免疫反应有关。     

PM2.5对血管内皮细胞氧化应激和凋亡的影响及机制

目的:从大气细颗粒物PM2.5对血管内皮细胞氧化应激和凋亡的影响,研究PM2.5对血管内皮细胞的毒性。方法:体外培养血管内皮细胞株EA.hy926,用不同浓度的PM2.5染毒24 h后,用CCK-8法测细胞的活性,用DCFH-DA荧光标记法检测细胞内氧自由基生成情况,用流式细胞术检测细胞凋亡率,然后用Western blot法检测凋亡相关蛋白细胞色素C、cleaved caspase-9和cleaved caspase-3的表达变化。结果:CCK-8法结果显示PM2.5对血管内皮细胞有明显的毒性,在浓度大于25 mg/L时可使EA.hy926细胞活性显著下降;PM2.5染毒24 h后可见DCFH-DA荧光染色增强,说明细胞内有大量的氧自由基形成;流式细胞术和Western blot检测证实PM2.5可以通过上调细胞色素C表达和活化cleaved caspase-9和cleaved caspase-3而诱导EA.hy926细胞凋亡。此外,用N-乙酰半胱氨酸抑制氧自由基生成可以抑制血管内皮细胞凋亡,提示PM2.5引起的细胞凋亡与氧化应激有关。结论:PM2.5可导致血管内皮细胞氧化应激水平增强和凋亡增加,这可能是其影响心血管系统功能的机制之一。     

应用组织芯片技术探讨"恶性组织细胞增生症"肿瘤细胞属性及其与EB病毒感染的关系

目的：初步探讨所谓“恶性组织细胞增生症”（简称恶组）肿瘤细胞的属性及其与EB病毒感染之间的关系。方法：用组织芯片技术将5例“恶组”尸检病例的每例不同组织各集成在一张组织芯片上,用免疫组织化学标记链霉素卵白素生物素（LSAB）法检测瘤细胞的免疫表型,用EBER1／2原位杂交检测Epstein-Barr(EB)病毒感染的情况。结果：（1）5例瘤细胞均表达CD45RO、CD3ε、T细胞限制性细胞内抗原－1（TIA－1）、Granzyme B,无瘤细胞表达CD56、CD30、CD20、CD68。（2）5例EBER1／2原位杂交均为阳性（簇型3例、弥漫型2例）。结论：至少部分“恶组”为EB病毒相关的侵袭性T细胞淋巴瘤。     

Differential post-translational modifications of microtubules in cells of the seminiferous epithelium of the rat: a light and electron microscope immunocytochemical study

The cells of the seminiferous epithelium of the rat testis are a rich source of microtubules and contain distinct microtubular structures such as the meiotic spindle and manchette. Microtubule diversity can be maintained by differential genetic expression of the multiple alpha- and beta-tubulin polypeptides or by tubulin monomer acetylation and detyrosination, post-translational modifications of alpha-tubulin. In the present analysis, antibodies that specifically recognize acetylated (antiacetylated), tyrosinated (anti-Tyr) and detyrosinated (anti-Glu) alpha-tubulins were employed to examine the distribution of post-translationally modified microtubules in the cells of the seminiferous epithelium. In the light microscope, a distinct pattern of staining for each antibody was detected using immunoperoxidase techniques on paraffin-embedded testicular sections. In the case of the anti-Glu antibody, a dense immunoperoxidase staining was detected in the cytoplasm of steps 4-7 spermatids. Thereafter, staining was noted over the area corresponding to the manchette of steps 8-15 spermatids, but not over their cytoplasm. The tails of spermatids were also reactive with this antibody. The anti-Tyr antibody was observed to be localized over the cytoplasm of Sertoli cells in their basal, supranuclear, and apical regions. A dense immunoperoxidase staining was also noted in the cytoplasm of pachytene spermatocytes, but it was negligible in the cytoplasm of spermatocytes undergoing their meiotic division; in these cells the centrioles and meiotic spindle were reactive. The spermatid's tails were also reactive. The antiacetylated antibody showed reactivity only over the tails of spermatids. With the electron microscope, a similar pattern of labeling was noted using immunogold labeling on Lowicryl K4M embedded testicular sections. The anti-Glu antibody heavily labeled microtubules of the manchette and the axoneme of tails of spermatids as well as microtubules of the proximal and distal centrioles and centriolar adjunct. The anti-Tyr antibody strongly labeled microtubules of Sertoli cells and the meiotic spindle and midbody of dividing spermatocytes. The anti-Tyr antibody also labeled the microtubules of the axoneme, centrioles, and centriolar adjunct of spermatids, but to a lesser degree than the anti-Glu antibodies; the manchette was faintly labeled. Of the three antibodies, the antiacetylated antibody showed the weakest labeling of microtubules of the centrioles, centriolar adjunct, and midbody, whereas those of the manchette and Sertoli cells were unreactive; the axoneme was moderately labeled.(ABSTRACT TRUNCATED AT 400 WORDS)     

Evidence for M2 macrophages in granulomas from pulmonary sarcoidosis: A new aspect of macrophage heterogeneity

Background

Sarcoidosis is a granulomatous disease of unknown etiology. Macrophages play a key role in granuloma formation with the T cells, having a significant impact on macrophage polarization (M1 and M2) and the cellular composition of the granuloma. This study evaluates macrophage polarization in granulomas in pulmonary sarcoidosis.

用免疫金银染色法和免疫电镜观察重组痘苗病毒对狂犬病毒糖蛋白的表达

用负染及超薄切片的方法电镜观察了表达狂犬病毒糖蛋白的重组痘苗病毒ＴＴＶ１１ＫＲＧ株（简称重组病毒）的纯度、形态与结构，显示重组病毒呈典型的砖形及卵圆形。用特异的抗狂犬病毒糖蛋白的单克隆抗体为一抗，胶体金标记的羊抗鼠ＩｇＧ为二抗，作免疫金银染色，在普通光学显微镜下显示该重组病毒感染的ＣＶ－１细胞膜上存在大量金银颗粒的吸附。进一步作胶体金免疫电镜，显示该感染细胞经金标后细胞膜上存在大量电子密度致密的金颗粒，从而直观地证实了该重组病毒在感染的宿主细胞膜上有大量狂犬病毒糖蛋白的表达。     

绿色荧光蛋白标记成人骨髓间充质干细胞的超微结构特征

背景：研究表明,绿色荧光蛋白标记的骨髓间充质干细胞免疫学表型、细胞周期、分化潜能等均未发生明显改变。 目的：进一步观察绿色荧光蛋白标记对骨髓间充质干细胞超微结构的影响。 方法：分离培养成人骨髓间充质干细胞,抗CD34、抗CD105免疫细胞化学染色鉴定,选第3代细胞进行绿色荧光蛋白标记,超薄切片后用透射电镜观察细胞超微结构,以未经绿色荧光蛋白标记骨髓间充质干细胞为对照。 结果与结论：骨髓间充质干细胞表达CD105,不表达CD34。绿色荧光蛋白标记后,骨髓间充质干细胞细胞质发出绿色荧光,绿色荧光主要集中于细胞核周围的胞浆内,远离细胞核的胞浆内荧光强度逐渐减弱。相对于未标记的骨髓间充质细胞,经绿色荧光蛋白标记后细胞粗面内质网、高尔基体等细胞器较多,而线粒体相对较少;另外,脂滴和“空泡”样结构也多一些。结果证实绿色荧光蛋白对骨髓间充质干细胞性状的影响较为局限,是一种较为理想的细胞标记示踪剂。     

Dendritic cells in muscle lesions of sarcoidosis

Sarcoidosis is a chronic systemic granulomatous disorder of unknown etiology. The precise mechanism by which granulomatous lesions form is still obscure. Dendritic cells (DCs) are the most efficient antigen presenting cells; however, pathologic investigations of dendritic cells in the affected lesions of sarcoidosis are quite limited. We immunohistochemically examined the localization and phenotypes of dendritic cells and the expressions of CD40 and CD40L (CD154), which are key molecules in dendritic cell activation, in the muscles of 5 patients with muscular sarcoidosis, 8 patients with muscular disorders without inflammation, and 4 patients with histologically normal muscles as controls. In muscular sarcoidosis, CD1c-positive myeloid dendritic cells were scattered mainly in the lymphocyte layers of granulomas and the endomysium around the granulomas. Double immunostaining revealed that some CD1c-positive cells expressed the mature dendritic cell marker CD83, but immature dendritic cell marker CD1a-positive cells were not found. Smaller numbers of Blood dendritic cell antigen (BDCA)-2-positive plasmacytoid dendritic cells were found in the lymphocyte layers of granulomas. In the controls, small numbers of CD1c-positive cells were seen in the endomysium, whereas BDCA-2-positive cells were not observed except in 1 case. In muscular sarcoidosis, CD40 was expressed on mononuclear cells, on the interstitium around the muscle fibers and granulomas, and on the endothelium of vessels. CD40L was positive on mononuclear cells scattered within and around granulomas in 3 of 5 patients. In the controls, CD40 was expressed on the endothelium of the vessels and sparse mononuclear cells in the lesions of muscle fiber necrosis, whereas CD40L was not seen in any. In muscular sarcoidosis, recruitment of myeloid dendritic cells and less plasmacytoid dendritic cells and up-regulation of the CD40/CD40L system in affected muscles suggest that myeloid dendritic cells may be mainly involved in granulomatous inflammation through antigen presentation in a Th1 immune milieu.     

5-氟尿嘧啶诱导人肺腺癌A549细胞自噬

目的 探讨5-氟尿嘧啶(5-FU)是否诱导人肺腺癌A549细胞发生自噬.方法 吖啶橙(AO)荧光染色和透射电镜观察自噬泡的变化;细胞免疫化学法测定LC3-Ⅱ的表达;流式细胞术及吖啶橙染色结合激光扫描共焦显微镜检测细胞凋亡;DNA电泳检测凋亡梯形条带的产生.结果 吖啶橙荧光染色和透射电镜观察结果显示,5-氟尿嘧啶处理细胞...     

Cryptococcal infection of the femoral bone similar with pathologic features of vascular tumors: a case report and review of literature

A rare case is presented of a 62-year-old man with primary isolated cryptococcal femoral osteomyelitis. Magnetic resonance imaging (MRI) revealed osteolytic destruction of his left femur. Biopsy was performed firstly. Under microscope, the lesion was compose of numerous large mononuclear cells, scattered multinucleated giant cells, a few lymphocytes and neutrophils, necrosis with serious artificial deformation. By immunohistochemistry (IHC), only CD31 and CD68 were positive, while CK, CK8/18, EMA, P63, CK7, CK20, PSAP, PSA, CD34 negative. It was considered a low grade vascularsarcoma, but not confirmed. Then the operation was done. Surgical specimen showed a lot of red-sphere materials in most cells cytoplasm. The Gomorra methenamine silver staining and PAS revealed the mucopolysaccharide-containing capsule of the Cryptococcus. Laboratory culture of lesion liquid grew a kind of yeast at 37°C. Cryptococcal femoral osteomyelitis was diagnosed at last. The patient is good now after the thorough debridement and anti-fungal treatment.     

Pregranulomatous phase of sarcoidosis: immunohistochemical diagnosis

Histopathological confirmation of clinical suspicion of sarcoidosis is based on the finding of non-caseating granulomas in biopsy material, usually in prescalene lymph nodes or in transbronchial lung biopsies. Lymph node reactive sinus histiocytosis (RSH) seen in relation to various inflammatory and non-inflammatory diseases can mimic the pregranulomatous phase of sarcoidosis (PSH). Differentiation of sinus histiocytosis based on histopathological features alone is limited. The purpose of this study is immunohistochemical determination of lymph node cellular response in granulomatous sarcoidosis, the PSH and RSH using a immunohistochemistry employing a panel of antibodies. Patient groups under study each contained 25 patients and included: those with clinical picture of sarcoidosis and non-caseating granulomatous lymphadenitis; those with confirmed sarcoidosis and with sinus histiocytosis without granuloma formation in lymph nodes; and finally, those without sarcoidosis and with “reactive” sinus histiocytois in lymph nodes. Lymph node biopsy tissue was fixed in buffered formaldehyde, routinely processed to paraffin wax blocks, cut into 4-μm-thick sections, stained with hematoxylin and eosin and immunohistochemically labelled using a triple-layer APAAP protocol with purified polyclonal antibodies directed against SP 70 and SP90 from Mycobacterium tuberculosis and monoclonal antibodies against CD22, CD4, CD8, CD56, and CD68. Intensity of immunolabelling was assessed semiquantitatively by two independent observers.

An increased CD4:CD8 ratio, moderate increase of immunolabelling for CD68 and slight decrease in immunolabelling for CD20, CD56, and SP90 was indicative of PSH when compared with RSH. The most notable difference between the studied groups was a difference in imunoreactivity to SP70 and CD4 antibodies. Lymph nodes with pregranulomatous sinus histiocytosis labelled with both antibodies. This profile of immunolabelling can be used in the differentiation of this condition from reactive sinusoidal lesions.     

The Macrophage Origin of the HIV-Expressing Multinucleated Giant Cells in Hyperplastic Tonsils and Adenoids

Replication and storage of virus are characteristic features of hyperplastic lymphoid tissues in HIV infection. In opportunistic infections, HIV is synthesized by phagocytic mononuclear and Langhans'-type multinucleated macrophages that coexpress the dendritic cell-associated S-100 and p55 antigens. However, similar cells in hyperplastic tonsils and adenoids from HIV+ individuals were alternatively identified as macrophages or, on the basis of the same S-100 and p55 staining, as dendritic cells. To consider establishing the role of these HIV-rich cells in HIV disease, it is important to reconcile this apparent discrepancy in identity. Hyperplastic tonsils and adenoid specimens were analyzed by HIV RNA in situ hybridization (ISH), light and transmission electron microscopy (TEM), and immunohistochemistry (IHC) (HIV Gag p24 protein, S-100, p55, CD68, HAM56, lysozyme, alpha -1-anti-trypsin, and alpha -1-antichymotrypsin). In HIV+ pediatric and adult surgical specimens (n=11), the giant cells and their mononuclear counterpart were positive for both macrophage and p55 and S-100 IHC markers. In addition, TEM, p24 IHC, and ISH showed HIV expression by cells with typical features of macrophages. Furthermore, these cells were not unique to HIV+ specimens, being seen in 20% of hyperplastic T&A surgical specimens (n=57) lacking HIV as well as in several types of granulomatous processes, such as sarcoidosis. These cells appear to represent an activated phenotype that can develop independent of HIV, but that may represent a viral host in HIV-infected individuals. Thus, the giant and mononuclear cells that produce striking amounts of HIV in tonsils and adenoids are of macrophage origin, yet, as in opportunistic infections, share dendritic cell-associated antigens, reflecting a common CD34+ bone marrow progenitor.