烫伤后肠壁组织T淋巴细胞和浆细胞数量的变化

目的：了解烧伤后肠壁组织T淋巴细胞和IgA浆细胞数量的变化与伤后肠道细菌易位及肠源性脓毒症发生、发展的关系。方法：Wistar大鼠50只，随机分成对照组（l只）和烫伤组（40只）。烫伤组动物背部脱毛，将背部浸于沸水中12秒钟，造成40％体表面积Ⅲ度烫伤，分别于伤后第1、3、7和10日处死，留取标本；对照组动物不烫伤，于处理后第1日处死，留取标本。采用免疫组化方法分别测定回肠固有层和粘膜层CD3 、CD4 和CD8 淋巴细胞以及IgA浆细胞数量，并测定肠道细菌IgA包被率和肠道细菌易位率。结果：伤后肠壁组织中CD3 、CD4 T淋巴细胞和lgA浆细胞的数量明显减少，CD4 ／CD8 比值和肠道细菌IgA包被率亦明显降低，而肠道细菌易位率则明显升高。结论：肠壁组织中T淋巴细胞和IgA浆细胞数量减少、肠道细菌IgA包被率降低与肠道细菌易位率升高有密切关系，其在烧伤后肠源性脓毒症的发生和发展中可能具有重要意义。     

脓毒症大鼠肠黏膜免疫屏障功能的变化

目的 研究脓毒症对大鼠肠黏膜免疫屏障功能的影响.方法 60只SD大鼠随机(随机数字法)分为对照组(n=15)和脓毒症组(n=45),采用盲肠结扎穿孔术(CLP)建立脓毒症模型.模型建立后3 h、6 h和12 h留取回肠黏膜和全血标本.分别进行肠黏膜形态学观察、肠防御素5(RD-5)及肠三叶因子3(TFF_3)Mrna表达水平检测、肠黏膜淋巴细胞凋亡分析,以及外周血中肠源性细菌DNA定性检测.结果 CLP所致脓毒症导致大鼠回肠黏膜明显损害,主要表现为上皮脱落、固有层分离、毛细血管出血和溃疡形成;脓毒症组模型建立后3 h即出现RD-5和TFF_3 Mrna表达显著性减少(与正常组比较,P<0.05),且6 h和12 h组进行下降(与3 h组比较,P<0.05),肠黏膜淋巴细胞凋亡数亦显著增加(P<0.05);同时,脓毒症组全血肠源性细菌DNA扩增全部阳性.结论 脓毒症时大鼠肠黏膜免疫屏障功能显著减退,且随脓毒症的发展而进行性恶化.     

α-黑素细胞刺激素对缺血再灌注损伤大鼠肠黏膜免疫功能的影响

目的 :探讨α 黑素细胞刺激素 (α MSH )对缺血再灌注 (I/R)损伤大鼠肠黏膜免疫屏障的保护作用及机制。方法 :采用大鼠小肠缺血 45min再灌注模型 ,治疗组于再灌注 5min内尾静脉注射α MSH。于再灌注后 2h用免疫放射法测定血清、肠黏膜组织中分泌型免疫球蛋白A (sIgA)的含量 ;四甲基偶氮唑盐微量酶反应比色法 (MTT)测定Peyer’s淋巴结 (PP)、上皮内淋巴细胞 (IEL)和固有层淋巴细胞 (LPL)增殖活力。结果 :肠I/R后血清和肠黏膜中sIgA含量下降 ,淋巴细胞增殖活性下降 (P <0 0 1) ;不同剂量的α MSH治疗组均能逆转I/R后sIgA含量下降和淋巴细胞增殖活力下降 ,差异有显著意义 (P <0 0 1) ,而不同剂量α MSH治疗组间各指标无显著性差异 (P >0 0 5 )。结论 :外源性α MSH可参与调节肠道相关淋巴组织免疫功能 ,对缺血再灌注损伤肠道免疫屏障具有保护作用     

大鼠肠缺血再灌注损伤后肠黏膜免疫功能的变化与意义

目的 :观察大鼠肠缺血再灌注损伤后肠黏膜免疫功能的变化 ,并探讨其与肠源性细菌内毒素移位的关系。方法 :采用大鼠小肠缺血 45min再灌注模型 ,分别于再灌注后即刻、2h、6h、2 4h用免疫放射法测定肠黏膜组织中分泌型免疫球蛋白A(sIgA)的含量 ;四甲基偶氮唑盐微量酶反应比色法 (MTT)测定Peyer’s淋巴结 (PP)、上皮内淋巴细胞 (IEL)和固有层淋巴细胞 (LPL)增殖活力 ;无菌取肠系膜淋巴结行细菌培养 ,统计细菌移位率 ;取门静脉血检测内毒素。结果 :肠缺血再灌注后肠黏膜中sIgA含量及淋巴细胞增殖活性均明显下降 (P <0 0 1) ,血浆内毒素含量较再灌注前显著升高 (P <0 0 1) ;并于再灌注后 2h起出现肠系膜淋巴结细菌移位 ;肠黏膜内sIgA含量及肠道相关淋巴组织淋巴细胞增殖活力与肠源性细菌内毒素移位呈显著负相关 (r =-0 5 5 3～ -0 75 3 ,P <0 0 1)。结论 :肠缺血再灌注损伤后肠黏膜免疫功能下降 ,与肠外细菌内毒素移位的发生密切相关。     

单核细胞趋化蛋白-1在溃疡性结肠炎黏膜中的表达

目的探讨单核细胞趋化蛋白-1(MCP-1)在溃疡性结肠炎(UC)发病机制中的作用。方法32例UC黏膜标本取自行结肠镜检查的患者,按病理组织学对炎症进行分级,Ⅲ、Ⅳ级20例,Ⅰ、Ⅱ级12例;对照组为15名健康成人。应用半定量RT-PCR检测对照组和UC组肠黏膜MCP-1 mRNA表达水平,免疫组织化学方法检测MCP-1蛋白的表达。结果与对照组相比,UC肠黏膜MCP-1 mRNA和其蛋白过度表达,MCP-1 mRNA表达与疾病严重程度成正相关(P<0.01)。MCP-1蛋白表达位于UC肠黏膜固有层单核细胞和T淋巴细胞,病理分级Ⅲ、Ⅳ级肠黏膜MCP-1蛋白表达较病理分级Ⅰ、Ⅱ级组明显增加(t=7.31,P<0.01)。结论UC黏膜组织中MCP-1表达水平明显上调,其表达水平与病情轻重和炎症严重程度呈正相关。     

免疫微生态营养对重症急性胰腺炎肠黏膜屏障功能及血清NETs水平的影响研究

目的探讨免疫微生态营养对重症急性胰腺炎(Severe acute pancreatitis,SAP)肠黏膜屏障功能及血清中性粒细胞胞外诱捕网(Neutrophil extracellular traps,NETs)水平的影响。方法以收治的72例SAP患者进行研究,循随机数字表法分为对照组及观察组,对照组予以常规肠内营养支持,观察组则施以免疫微生态营养支持方案,均持续治疗14 d,比较两组肠黏膜屏障功能及NETS水平、免疫指标水平及预后情况。结果治疗后,两组内毒素、D-乳酸及NETS水平均呈下降趋势,且观察组低于对照组(P<0.05);两组CD4^(+)T细胞、IgA及IgM水平均升高,CD8^(+)T细胞水平降低,且观察组CD4^(+)T细胞、IgA及IgM水平高于对照组,CD8^(+)T细胞水平低于对照组(P<0.05);两组并发症无明显差异(P>0.05);两组APACHEⅡ评分均降低,且观察组低于对照组(P<0.05)。结论SAP患者给予免疫微生态营养支持,可较快缓解临床症状,减轻炎症反应,有利于肠黏膜屏障功能及NETS水平改善,免疫功能有所增强,且可获较好预后。     

肠淋巴细胞归巢及中医药干预相关性研究

<正>肠淋巴细胞归巢相关概念肠道是机体最大的免疫器官,通过其免疫监视和免疫应答功能,坚守着肠黏膜免疫屏障(gut mucosal immunobarrier),能够在肠黏膜发挥免疫效应的淋巴细胞是从流动血液中定向迁移(traffic)到黏膜部位的淋巴细胞,即通过肠淋巴细胞归巢(lymphocyte homing)而来,可以说,淋巴细胞归巢过程的正常决定了肠黏膜免疫屏障功能的坚固[1~2]。循环血液中的淋巴细胞之所以能够定向归巢到肠道而不是其他部位,是因为在     

四君子汤修复烧伤后肠黏膜屏障的超微结构变化

目的:通过烧伤动物模型的建立,观察四君子汤煎剂对肠黏膜屏障的影响及产生机制.方法:用大鼠作为研究对象,随机抽样,平均分组.正常对照组不做处理;烧伤对照组管饲蒸馏水;烧伤试验组管饲中药煎剂.结果:烧伤对照组肠黏膜上皮变性、坏死,炎症明显,黏膜屏障功能受损严重.结论:四君子汤具有明显早期保护严重烧伤后肠黏膜的屏障功能.     

丙氨酰谷氨酰胺对创伤后肠粘膜屏障的修复作用研究

目的：利用SPF大鼠模型，观察失血后低血容量性休克后全胃肠外营养（TPN）、TPN液中添加Ala－Gln（TPN加Ala－Gln）和经口进食（TEN）3种营养模式对肠粘膜免疫系统、肠粘膜菌群双歧杆菌／大肠杆菌比值和血浆内毒素（LPS）水平的影响，探讨Ala－Gln是否对损伤后肠粘膜屏障有修复作用。方法：24只SPFWistar大鼠实施失血后低血容量性休克，复苏后以TPN、TPN加Ala－Gln和TEN3种营养方式支持7日后剖杀。以回肠内容物细菌S－IgA包被率、肠固有层淋巴细胞和浆细胞计数、回肠革兰氏阴性细菌粘附率及血浆LPS水平为观察指标。结果：上述各项指标在TEN组变化最轻；，在TPN组变化最重，表现为肠固有层CD3 、CD4 、CD8 淋巴细胞和IgA浆细胞明显减少，肠腔细菌S－lgA包被率下降，肠道微生态发生紊乱，细菌粘附率和易位率上升，血浆LPS水平升高，死亡率高；TPN加Ala－Gln组各参数接近TEN组。结论：标准TPN能削弱肠粘膜免疫系统，加重粘膜屏障损伤；而适量补充Ala－Gln能减轻这种损害，有利于肠粘膜屏障的修复。     

腹部开放伤后海水浸泡对大鼠肠屏障和传输功能的影响

目的:探讨大鼠腹部开放伤后海水浸泡对肠屏障和传输功能的影响,为研究肠道损伤及其保护提供依据.方法:建立腹部开放伤合并海水浸泡大鼠模型,测定血二胺氧化酶(DAO)、D-乳酸、内毒素(LPS)、肿瘤坏死因子-α(TNF-α)含量;测定肠内容物SIgA及血IgA含量;测定小肠蠕动速率变化;观察小肠组织病理变化.结果:腹部开放伤后海水浸泡大鼠血DAO、D-乳酸、LPS、TNF-α含量较正常时照组均显著升高(P＜0.01):肠内容物SIgA、血IgA含量较正常对照组显著下降(P＜0.01);小肠蠕动速率显著下降(P＜0.01);小肠黏膜病理损伤显著.结论:腹部开放伤后海水浸泡可致大鼠肠屏障和传输功能受损,成为伤后肠源性感染及多脏器功能障碍综合征发生的原因之一.     

Gut ischemia-reperfusion affects gut mucosal immunity: a possible mechanism for infectious complications after severe surgical insults

OBJECTIVE: To examine influences of gut ischemia/reperfusion (I/R) on gut-associated lymphoid tissue (GALT) mass and function. DESIGN: Prospective, randomized controlled study. SETTING: Research laboratory. SUBJECTS: Male Institute of Cancer Research mice. INTERVENTIONS: Ninety mice were randomized to three groups: I/R (60-min gut ischemia), sham (laparotomy only), and control (no operation). On days 1, 2, 4, 7, and 10, mice were killed to harvest lymphocytes from Peyer patches, the intraepithelial space, and the lamina propria (LP) of the small intestine. Respiratory tract and small intestinal washings were also obtained. MEASUREMENTS AND MAIN RESULTS: Gut I/R significantly reduced lymphocyte numbers in Peyer patches, the intraepithelial space, and the LP. The reduction was prominent in GALT effector sites, that is, the intraepithelial space and LP, but numbers recovered quickly in LP. Changes in cell numbers in Peyer patches, GALT inductive sites, were subtle but persistent. Gut I/R reduced B cell numbers in Peyer patches; alphabeta T cell receptor (TCR)+, gammadeltaTCR+, CD8+, and B cell numbers in the intraepithelial space; and gammadeltaTCR+, CD8+, and B cell numbers in the LP, in comparison with the sham or control group. There were no significant differences in respiratory tract immunoglobulin A levels between the I/R and sham groups. Intestinal immunoglobulin A was elevated on day 1 in the I/R group, with no significant difference after day 2 in comparison with the sham group. CONCLUSIONS: Despite the maintained mucosal immunoglobulin A level, gut I/R markedly reduces GALT cell numbers, with changes in lymphocyte phenotypes. These alterations may be associated with increased morbidity due to infectious complications after severe surgical insults.     

Decreased lymphocyte apoptosis by anti-tumor necrosis factor antibody in Peyer's patches after severe burn

Severe burn results in immunosuppression, with increased lymphocyte apoptosis in both the central and peripheral immune system. As atrophy of the small intestine has been described in mouse models and intestinal lymphocytes have been implicated in the burn inflammatory response, we examined the effects of burn and tumor necrosis factor (TNF)-alpha on lymphocytes in intestinal Peyer's patches. Anesthetized C57BL6 mice received a 30% full-thickness scald burn on the upper back. Sham-burned animals served as controls. Anti-TNF or control immunoglobulin (Ig) G antibody (200 microg) was given immediately after the burn. The animals were initially resuscitated with 2 mL of normal saline, and were then sacrificed 12 h postburn. Terminal deoxyuridine nick-end labeling (TUNEL) and proliferative cell nuclear antigen (PCNA) staining was performed. Apoptosis was quantified as apoptotic lymphocytes/high-powered field (hpf). Results, expressed as mean +/- SEM, were compared using analysis of variance (ANOVA) and the Student-Newman-Keuls test. All mice survived the burn. An initial time-course experiment demonstrated maximal Peyer's patch apoptosis 12 h after the burn. Sham mice had 25 +/- 7 TUNEL-stained cells/hpf in Peyer's patches, whereas burned mice had 93 +/- 18 cells/hpf (P < 0.05). In contrast, burned mice receiving anti-TNF antibody had 28 +/- 8 TUNEL-stained cells/hpf (P < 0.05 vs. burn), whereas sham mice receiving anti-TNF antibody had 20 +/- 4 cells/hpf. There were no significant differences in PCNA staining between the groups. Scald burn results in lymphocyte apoptosis in Peyer's patches. This apoptosis can be abrogated by the addition of anti-TNF antibody. Apoptotic changes may lead to the failure of the intestinal immunological barrier and increased risk of sepsis.     

亚低温缺血预处理对大鼠肠缺血再灌注诱导细胞凋亡的保护

背景细胞凋亡在肠缺血再灌注损伤中起关键性作用,细胞凋亡的发生与凋亡抑制基因Bcl-2和凋亡促进基因Bax蛋白表达程度密切相关.目的探讨亚低温缺血预处理对大鼠肠组织缺血再灌注后凋亡相关基因Bcl-2和Bax蛋白表达的影响.设计随机对照实验.单位湖北省咸宁学院医学院外科学教研室与生物化学教研室.材料实验于2002-04/12在咸宁学院医学院中心实验室完成.选用Wistar健康雄性大鼠32只,术前禁食24 h,自由饮水.随机分为假手术对照组、缺血再灌注组、缺血预处理组、亚低温预处理组,8只/组.方法除假手术对照组外,其余3组建立缺血再灌注模型.①假手术对照组仅暴露肠系膜上动脉而不夹闭,共2 h,结束实验后取材;缺血再灌注组夹闭肠系膜上动脉60min后松夹60 min再取材;缺血预处理组夹闭肠系膜上动脉5 min和松夹5 min作为预处理,余同缺血再灌注组;亚低温预处理组实施缺血预处理前在小肠周围充填碎冰造成小肠亚低温(33～35℃),余同缺血预处理组.②各组大鼠取中段小肠4 cm,分为两段,分别置于甲醛和戊二醛中固定,制作电镜标本.免疫组化后显微镜下用图像分析系统检测各组吸光度值,每组选10个视野进行测量,计算平均值,肠黏膜损伤按Chiu标准进行分级.0级正常黏膜绒毛;Ⅰ级上皮下间隙增大,通常在绒毛的尖端,常伴有毛细血管淤血;Ⅱ级上皮下间隙扩张伴随上皮层同固有层中度分离;Ⅲ级绒毛两侧上皮层大量的同固有层分离,部分绒毛顶端破损;Ⅳ级绒毛破损伴随固有层毛细血管暴露,可能观察到固有层的细胞成分增多;Ⅴ级固有层破坏和不完整、出血和溃疡.主要观察指标①各组肠缺血再灌注后Bcl-2与Bax蛋白吸光度值的变化.②各组肠黏膜损伤分级.③各组肠黏膜组织学变化.结果32只大鼠全部进入结果分析,中途无脱落.①各组肠缺血再灌注后Bcl-2与Bax蛋白吸光度值的变化与假手术对照组比较,缺血再灌注组均明显升高(4.03±1.02,9.56±1.32,P＜0.01;5.67±1.34,19.07±1.63,P＜0.01);与缺血再灌注组比较,缺血预处理组Bcl-2表达升高(9.56±1.32,15.03±1.44,P＜0.01),Bax表达降低(19.07±1.63,14.11±1.21,P＜0.01);与缺血预处理组比较,亚低温预处理组Bcl-2表达仍有所升高(15.03±1.44,18.17±2.03,P＜0.05),Bax表达仍降低(14.11±1.21,11.58±1.04,P＜0.05).②各组肠黏膜损伤分级情况假手术对照组肠黏膜基本正常,损伤均为0级;缺血再灌注组肠黏膜损伤Ⅱ级2只,Ⅲ级3只,Ⅳ级3只,明显高于假手术对照组(P＜0.01);缺血预处理组肠黏膜损伤Ⅰ级2只,Ⅱ级4只,Ⅲ级2只,明显低于缺血再灌注组(P＜0.01);亚低温预处理组肠黏膜损伤0级1只,Ⅰ级3只,Ⅱ级4只,低于缺血预处理组(P＜0.05).③各组肠黏膜组织学形态电镜观察结果假手术对照组肠黏膜上皮微绒毛排列整齐,各细胞器形态正常;缺血再灌注组肠黏膜上皮微绒毛稀疏、变短、脱落,线粒体明显肿胀,空泡变性,内质网排列紊乱、肿胀;缺血预处理组肠黏膜上皮微绒毛排列基本整齐,线粒体内质网轻度肿胀;而亚低温预处理组肠黏膜上皮微绒毛排列整齐,线粒体内质网肿胀不明显.结论肠缺血再灌注前进行缺血预处理可以上调Bcl-2蛋白的表达,并下调Bax蛋白的表达,从而抑制肠缺血再灌注诱导的细胞凋亡以保护缺血再灌注肠损伤.亚低温状态能增强缺血预处理的保护作用.     

沙参麦冬汤对运动小鼠免疫功能的影响*

目的:探讨沙参麦冬汤对运动小鼠免疫功能的影响。方法:40只雄性昆明种小鼠,随机分为4组：安静对照组、运动对照组、运动+小剂量沙参麦冬汤组、运动+大剂量沙参麦冬汤组,运动小鼠递增负荷游泳训练40d,游泳时间由40min开始渐增至100min,第40天游泳至力竭,24h后处死取血。测定小鼠免疫器官脏器/体重比值、外周血免疫球蛋白、外周血T细胞亚群。结果：服药组小鼠脾指数、外周血IgG、IgA、CD4+T细胞百分比、CD4+/CD8+比值均显著高于运动对照组(P<0.01或P<0.05);大剂量组小鼠胸腺指数、     

Exogenous interleukin 7 affects gut-associated lymphoid tissue in mice receiving total parenteral nutrition

In the absence of enteral nutrient delivery, gut-associated lymphoid tissue (GALT) mass and function are reduced. The purpose of this study was to examine whether exogenous interleukin (IL)-7 treatment reverses intravenous (IV)-total parenteral nutrition (TPN)-induced changes in GALT, immunoglobulin (Ig) A levels, and gut barrier function. Eighty-nine mice were randomized to chow, TPN, or TPN + IL-7 (1 microg/kg, administered IV twice a day) and treated for 5 days. The entire small intestine was harvested and lymphocytes were isolated from Peyer's patches (PPs), intraepithelial (IE) spaces, and the lamina propria (LP). Small intestinal and bronchoalveolar IgA levels were measured. Proximal and distal small intestinal levels of IgA-stimulating (IL-10) and IgA-inhibiting (IFNgamma) cytokines were determined with enzyme-linked immunoabsorbant assay. Moreover, 1 x 10 live Pseudomonas aeruginosa were delivered by gavage and survival was observed. TPN decreased total cell yields from PPs, IE spaces, and the LP compared with the chow group. IL-7 treatment restored cell numbers. PP CD4+, PP CD8+, IE gammadeltaTCR+, and LP CD4+ cell numbers were higher in the TPN + IL-7 group than in the TPN group. Secretory IgA levels were lower in the TPN and TPN + IL-7 than in the chow group. In the distal small intestine, IFNgamma levels were similar in the three groups, whereas IL-10 levels were reduced in the TPN and TPN + IL-7 groups relative to the chow group. Survival times were reduced in the TPN compared with the chow group, but IL-7 treatment significantly improved survival. Thus, exogenous IL-7 does not improve secretory IgA levels, nor are there any remarkable effects on levels of gut IgA-mediating cytokines. However, IL-7 treatment during TPN reverses TPN-induced GALT atrophy and improves survival in a gut-derived sepsis model.     

Ontogenetic aspects of the intestinal immune system in man

Summary The development of the mucosal immune system in the human fetus has been studied in some detail. Aggregates of T and B cells form early Peyer's patches by 16 weeks gestation and by 19 weeks organised Peyer's patches with T and B cell zones are seen. T cells populate the mucosal lamina propria and epithelium from 11 weeks gestation and increase in number thereafter. As in the adult, most intraepithelial lymphocytes are CD8⁺ and most lamina propria T cells are CD4⁺. By 20 weeks, villus epithelial cells are HLA-DR⁺ and secretory component is also expressed. In the absence of lumenal stimulation in the fetus there is no intestinal secretory IgA antibody response. A few IgA plasma cells are present in fetal salivary glands but the number does not dramatically increase until after birth.     

Ontogenetic aspects of the intestinal immune system in man

Summary The development of the mucosal immune system in the human fetus has been studied in some detail. Aggregates of T and B cells form early Peyer's patches by 16 weeks gestation and by 19 weeks organised Peyer's patches with T and B cell zones are seen. T cells populate the mucosal lamina propria and epithelium from 11 weeks gestation and increase in number thereafter. As in the adult, most intraepithelial lymphocytes are CD8⁺ and most lamina propria T cells are CD4⁺. By 20 weeks, villus epithelial cells are HLA-DR⁺ and secretory component is also expressed. In the absence of lumenal stimulation in the fetus there is no intestinal secretory IgA antibody response. A few IgA plasma cells are present in fetal salivary glands but the number does not dramatically increase until after birth.     

Ontogenetic aspects of the intestinal immune system in man

Summary The development of the mucosal immune system in the human fetus has been studied in some detail. Aggregates of T and B cells form early Peyer's patches by 16 weeks gestation and by 19 weeks organised Peyer's patches with T and B cell zones are seen. T cells populate the mucosal lamina propria and epithelium from 11 weeks gestation and increase in number thereafter. As in the adult, most intrepithelial lymphocytes are CD8⁺ and most lamina propria T cells are CD4⁺. By 20 weeks, villus epithelial cells are HLA-DR⁺ and secretory component is also expressed. In the absence of lumenal stimulation in the fetus there is no intestinal secretory IgA antibody response. A few IgA plasma cells are present in fetal salivary glands but the number does not dramatically increase until after birth.     

Ontogenetic aspects of the intestinal immune system in man

Summary The development of the mucosal immune system in the human fetus has been studied in some detail. Aggregates of T and B cells form early Peyer's patches by 16 weeks gestation and by 19 weeks organised Peyer's patches with T and B cell zones are seen. T cells populate the mucosal lamina propria and epithelium from 11 weeks gestation and increase in number thereafter. As in the adult, most intraepithelial lymphocytes are CD8⁺ and most lamina propria T cells are CD4⁺. By 20 weeks, villus epithelial cells are HLA-DR⁺ and secretory component is also expressed. In the absence of lumenal stimulation in the fetus there is no intestinal secretory IgA antibody response. A few IgA plasma cells are present in fetal salivary glands but the number does not dramatically increase until after birth.