Functions of follicular and marginal zone B cells in pregnancy

Dear Editor, Pregnancy is a physiological condition when immune cells face a dual crisis, as on one hand, the body needs to essentially tolerate semi-allogenic fetus possessing antigens from maternal and paternal sides, while on the other hand the maternal as well as the fetal body must not be adversely affected by infections. This delicate balance between immune tolerance and responses is regulated by an orchestra of immune cells. Various immune regulations by B cells are lately being explored. These include the production of asymmetric antibodies, induced by pregnancy factors, providing protection against maternally derived antipaternal symmetric antibodies at the feto-maternal interface[1] to protect the fetus from immune attack by destructive maternal natural killer cells as well as cytotoxic lymphocytes(2)Moreover, the regulatory B cells can inhibit pro-inflammatory responses triggered by T cells and pro inflammatory mediators during pregnancy, by secreting interleukin-10, a potent anti-inflammatory cytokine(3)Interleukin-10, secreted by B cells, also suppresses activities of the dendritic cells and keeps them in an immature state as mature dendritic cells would induce T cells which are detrimental to pregnancy sustenance[4].

Two distinct subpopulations of marginal zone B cells exhibit differential antibody-producing capacities and radioresistance

Marginal zone(MZ)B cells,which are splenic innate-like B cells that rapidly secrete antibodies(Abs)against blood-borne pathogens,are composed of heterogeneous subpopulations.Here,we showed that MZ B cells can be divided into two distinct subpopulations according to their CD80 expression levels.CD80^(high)MZ B cells exhibited greater Ab-producing,proliferative,and IL-10-secreting capacities than did CD80^(low)MZ B cells.Notably,CD80^(high)MZ B cells survived 2-Gy whole-body irradiation,whereas CD80^(low)MZ B cells were depleted by irradiation and then repleted with one month after irradiation.Depletion of CD80^(low)MZ B cells led to accelerated development of type II collagen(CII)-induced arthritis upon immunization with bovine CII.CD80^(high)MZ B cells exhibited higher expression of genes involved in proliferation,plasma cell differentiation,and the antioxidant response.CD80^(high)MZ B cells expressed more autoreactive B cell receptors(BCRs)that recognized double-stranded DNA or CII,expressed more immunoglobulin heavy chain sequences with shorter complementarity-determining region 3 sequences,and included more clonotypes with no N-nucleotides or with B-1a BCR sequences than CD80^(low)MZ B cells.Adoptive transfer experiments showed that CD21^(+)CD23^(+)transitional 2 MZ precursors preferentially generated CD80^(low)MZ B cells and that a proportion of CD80^(low)MZ B cells were converted into CD80^(high)MZ B cells;in contrast,CD80^(high)MZ B cells stably remained CD80^(high)MZ B cells.In summary,MZ B cells can be divided into two subpopulations according to their CD80 expression levels,Ab-producing capacity,radioresistance,and autoreactivity,and these findings may suggest a hierarchical composition of MZ B cells with differential stability and BCR specificity.

Function and regulation of self-reactive marginal zone B cells in autoimmune arthritis

Polyreactive innate-type B cells account for many B cells expressing self-reactivity in the periphery. Improper regulation of these B cells may be an important factor that underlies autoimmune disease. Here we have explored the influence of self-reactive innate B cells in the development of collagen-induced arthritis （CIA）, a mouse model of rheumatoid arthritis. We show that splenic marginal zone （MZ）, but not B- 1 B cells exhibit spontaneous IgM reactivity to autologous collagen II in na＇=＇ve mice. Upon immunization with heterologous collagen II in complete Freund＇s adjuvant the collagen-reactive MZ B cells expanded rapidly, while the B-1 B cells showed a modest anti-collagen response. The MZ B cells were easily activated by toll-like receptor （TLR） 4 and 9-1igands in vitro, inducing proliferation and cytokine secretion, implying that dual engagement of the B-cell receptor and TLRs may promote the immune response to self-antigen. Furthermore, collagen-primed MZ B cells showed significant antigen-presenting capacity as reflected by cognate T-cell proliferation in vitroand induction of IgG anti-collagen antibodies in vivo. MZ B cells that were deficient in complement receptors I and 2 demonstrated increased proliferation and cytokine production, while Fcy receptor lib deficiency of the cells lead to increased cytokine production and antigen presentation. In conclusion, our data highlight self-reactive MZ B cells as initiators of the autoimmune response in CIA, where complement and Fc receptors are relevant in controlling the self-reactivity in the cells.

Marginal zone B cells are naturally reactive to collagen type II and are involved in the initiation of the immune response in collagen-induced arthritis

Antibodies against type II collagen(CII)are essential for development of collagen-induced arthritis(CIA),but how and where the B-cell response to CII is initiated is not fully known.We show here that naive DBA/1 mice display naturally reactive IgM and IgG anti-CII producing B cells prior to immunization.The CII-reactive B cells were observed in the spleen and recognized as marginal zone(MZ)B cells.After CII immunization,CII-specific B cells expanded rapidly in the spleen,in contrast to the lymph nodes,with the initial response derived from MZ B cells and later by follicular(FO)B cells.This was evident despite that the MZ B cells were subject to stringent tolerance mechanisms by having a greater Fc gamma receptor IIb expression than the FO B cells.Further,the MZ B cells migrated to the FO areas upon immunization,possibly providing antigen and activating FO T cells and subsequently FO B cells.Thus,around CIA onset increased numbers of IgG anti-CII producing FO B cells was seen in the spleen,which was dominated by IgG2a-and IgG2b-positive cells.These data demonstrate that CII-reactive MZ B cells are present before and expand after CII immunization,suggesting an initiating role of MZ B cells in the development of CIA.

原发性皮肤边缘区B细胞淋巴瘤1例

报告原发性皮肤边缘区B细胞淋巴瘤1例。患者男,23岁,因背部红色结节5年就诊。皮肤科检查:背部多发大小不一红色结节,约5 mm×5 mm~10 mm×15 mm,表面光滑,边界清,未见明显鳞屑,质地较软,无压痛。皮损组织病理示:真皮层及皮下组织淋巴组织增生呈结节状分布,部分滤泡萎缩,其周围及小汗腺周围可见小-中等的中心细胞样及单核细胞样细胞围绕,局部侵及皮下脂肪组织。免疫组化示:CD20(+)、CD21(FDC网+)、CD23(FDC网+)、kappa(+)、Bcl-2(+)、CD43(部分+)、Ki-67(10%+),CD3、CD4、CD5、CD8、Lambda、Bcl-6、Cyclin-D1均阴性。诊断:原发性皮肤边缘区B细胞淋巴瘤。患者放弃治疗,1年后失访。

Role of non-Helicobacter pylori gastric Helicobacters in helicobacter pylori-negative gastric mucosa-associated lymphoid tissue lymphoma

Marginal zone lymphomas rank as the third most prevalent form of non-Hodgkin B-cell lymphoma,trailing behind diffuse large B-cell lymphoma and follicular lymphoma.Gastric mucosa-associated lymphoid tissue lymphoma(GML)is a low-grade B-cell neoplasia frequently correlated with Helicobacter pylori(H.pylori)-induced chronic gastritis.On the other hand,a specific subset of individuals diagnosed with GML does not exhibit H.pylori infection.In contrast to its H.pylori-positive counterpart,it was previously believed that H.pylori-negative GML was less likely to respond to antimicrobial therapy.Despite this,surprisingly,increasing evidence supports that a considerable proportion of patients with H.pylori-negative GML show complete histopathological remission after bacterial eradication therapy.Nonetheless,the precise mechanisms underlying this treatment responsiveness are not yet fully comprehended.In recent years,there has been growing interest in investigating the role of non-H.pylori gastric helicobacters(NHPHs)in the pathogenesis of H.pylori-negative GML.However,additional research is required to establish the causal relationship between NHPHs and GML.In this minireview,we examined the current understanding and proposed prospects on the involvement of NHPHs in H.pylori-negative GML,as well as their potential response to bacterial eradication therapy.

边缘区淋巴瘤转化为大B细胞淋巴瘤1例并文献复习

目的探讨黏膜相关淋巴组织结外边缘区淋巴瘤转化为弥漫大B细胞淋巴瘤病人的临床诊断和治疗。方法回顾1例原发性淋巴瘤黏膜相关淋巴组织结外边缘区淋巴瘤治疗缓解后出现弥漫大B细胞淋巴瘤转化病人的临床资料,分析其临床表现、治疗经过及预后,并复习相关文献。结果病人确诊直肠黏膜相关淋巴组织结外边缘区淋巴瘤后,给予R-CHOP方案(利妥昔单抗+环磷酰胺+多柔比星+长春新碱+泼尼松)化疗10疗程后淋巴瘤部分缓解;口服来那度胺维持半年后出现盆腔弥漫大B细胞淋巴瘤转化,考虑淋巴瘤进展,再次给予9疗程R-CHOP方案化疗;后出现中枢神经系统、肾上腺及淋巴结浸润,鞘内注射甲氨蝶呤+阿糖胞苷+地塞米松及大剂量甲氨蝶呤+利妥昔单抗化疗3疗程达部分缓解;后行自体造血干细胞移植治疗后淋巴瘤达完全缓解。口服伊布替尼单药维持治疗至今,现持续缓解3年余。结论R-CHOP方案化疗基础上的自体造血干细胞移植及伊布替尼单药维持治疗,对发生弥漫大B细胞淋巴瘤组织转化的黏膜相关淋巴组织结外边缘区淋巴瘤病人有良好的治疗效果。

SPARC基因缺失对小鼠脾脏边缘区B细胞抗凋亡机制影响的初步探讨

目的:探讨富含半胱氨酸的酸性分泌蛋白(SPARC)的基因缺失对小鼠脾脏边缘区B细胞抗凋亡机制的影响。方法:10只对SPARC缺失纯合的小鼠指定为缺失组,从对SPARC缺失杂合的小鼠杂交获得。10只野生型(WT)小鼠设置为WT组。小鼠常规饲养到4个月,行小鼠称重和脾脏称重以计算脾脏指数。每组收集5只小鼠脾脏,通过苏木精-伊红染色计算脾脏中白浆的面积百分比。每组5只小鼠脾脏,通过流式细胞术筛选脾边缘区B细胞。结果:缺失组的脾脏质量、脾脏指数、白浆面积百分比和边缘区B细胞百分比均显著高于WT组(P<0.05)。缺失组的体质量低于WT组(P<0.05)。两组在不同时间和相互作用,边缘区B细胞凋亡、Caspase8 mRNA和相对蛋白表达差异均有统计学意义(P<0.05)。缺失组的边缘区B细胞凋亡率、Caspase8 mRNA和蛋白质表达水平均低于WT组(P<0.05)。结论:SPARC基因缺失可引起脾肿大和边缘区B细胞增生,降低脾脏边缘区B细胞凋亡率,可能与SPARC基因缺失导致Caspase8 mRNA和蛋白的异常低表达水平有关。

眼结膜黏膜相关淋巴组织边缘带B细胞淋巴瘤临床病理分析

目的 探讨眼结膜黏膜相关淋巴组织边缘带B细胞淋巴瘤（marginal zone B cell lymphoma of mucosa-associated lymphoidtissue）（简称为MALT淋巴瘤）的临床病理特征、治疗及预后。方法 对15例眼结膜MALT淋巴瘤患者的临床病理资料进行回顾性分析及随访,复查和完善HE及免疫组化染色切片,4例进行Ig基因重排克隆性分析。结果 （1）15例患者中,男性5例,女性10例,中位年龄42岁,病史平均20个月。（2）病理形态：黏膜下大量密集淋巴样细胞弥漫浸润,并有模糊淋巴滤泡样结节。浸润细胞多为小～中等大小的淋巴样细胞及单核样B细胞。（3）免疫表型：浸润细胞CD20、CD79a、BCL-2均（＋）,CD3、CD5、CD10、Cyclin D1、TdT均（-）。（4）Ig基因克隆性分析：4例均呈单克隆。（5）随访：随访时间2～35个月,截止随访日期,所有患者均生存,且病变无复发。结论 眼结膜MALT淋巴瘤好发于中年女性,结膜红肿突起为主要特征,镜下以小细胞样边缘带B细胞为主,具有典型MALT淋巴瘤的免疫表型和惰性临床经过,预后良好。

天然角蛋白自身反应性B细胞亚群及功能的分析

目的:明确天然角蛋白反应性B细胞的亚群及解剖定位,初步分析其分泌天然抗角蛋白自身抗体(anti-keratinautoantibody,AKautoAb)的能力。方法:取SPF级C57BL/6小鼠的脾细胞和腹腔细胞,荧光抗体染色后用流式细胞仪分析角蛋白反应性B细胞亚群。将脾脏和腹腔淋巴细胞体外培养后,用ELISA分析AKautoAb的滴度,用ELISPOT法分析分泌AKautoAb的B细胞数。结果:腹腔中几乎所有结合角蛋白的B细胞均为B-1a细胞,脾脏中结合角蛋白的B细胞以边缘带B细胞为主。腹腔细胞中分泌AKautoAb的细胞数显著多于脾细胞,其培养上清中AKautoAb的滴度显著高于脾细胞。结论:角蛋白反应性B细胞存在于3个成熟B细胞亚群:B-1细胞、滤泡B细胞和边缘带B细胞,其中CD5+的B-1a细胞具有活跃的分泌AKautoAb的能力。

原发性皮肤边缘区B细胞淋巴瘤临床病理特征

目的探讨原发皮肤边缘区B细胞淋巴瘤(PCMZL)的临床和病理学特征,诊断和鉴别诊断。方法对2例PCMZL和1例皮肤淋巴组织增生(CLP)病例进行临床特征、组织形态学、免疫表型及PCRIgH基因重排分析。结果免疫组化示2例PCMZL的小淋巴细胞CD20和CD79α(),bcl-2、BOB.1和Oct-2(),MUM-1(+),CD5、CD10、bcl-6和CD23(-);浆细胞CD138、MUM-1(),限制性表达轻链kappa。1例CLP的小淋巴细胞CD20、CD3和bcl-2(),MUM1(+);浆细胞同时表达κ及λ。IgH扩增2例PCMZL呈单克隆性,1例CLP显示多克隆性。结论PCMZL属MALT-L家族,形态学上肿瘤细胞由异源性小淋巴细胞组成,免疫学上显示后生发中心标记。浆细胞轻链限制性和B细胞抗原受体基因克隆性重排对诊断有非常重要的帮助。

原发性肺结外边缘区B细胞淋巴瘤九例临床病理分析

目的 探讨原发性肺结外边缘区B细胞淋巴瘤 (primarypulmonaryextranodalmarginalzoneB celllymphoma ,即黏膜相关淋巴瘤 ,mucosa associatedlymphoidtissuelymphoma ,MALT淋巴瘤 )的临床病理特征和免疫组织化学 (immunohistochemistry ,IHC)染色 ,及其诊断和预后。 方法 对 9例原发性肺结外边缘区B细胞淋巴瘤进行临床病理、免疫组织化学 (LCA、CD2 0、CD45RO、κ、λ、Ki 67、CD5、cyclinD1、CK、NSE)分析。结果 结合免疫组织化学染色及病理组织形态 ,按淋巴造血组织肿瘤 2 0 0 1年新WHO分类 ,9例均被确诊为原发性肺结外边缘区B细胞淋巴瘤 (MALT淋巴瘤 )。本组男 4例 ,女 5例 ,男女之比为 1∶1.2 5 ;中位年龄 5 1.5岁。所有MALT淋巴瘤病例都呈LCA阳性、CD2 0阳性 ,Ki 67阳性率低 ;免疫球蛋白轻链限制性λ或κ阳性表达者分别为 5例、1例 ,κ和λ均阳性表达者 1例 ,2例无轻链限制性表达 ;CD45RO、CD5、cyclinD1、CK、NSE均阴性。结论 原发性肺结外边缘区B细胞淋巴瘤属惰性淋巴瘤 ,临床极易误诊 ,必须结合其病理组织形态和免疫组织化学染色进行诊断和鉴别诊断。

惰性B细胞非霍奇金淋巴瘤与肝炎病毒感染相关性分析

目的:分析惰性B细胞非霍奇金淋巴瘤(B cell non-Hodgkin lymphoma,B-NHL)不同亚型患者乙型肝炎病毒(hepatitis B virus,HBV)及丙型肝炎病毒(hepatitis C virus,HCV)感染的情况,探讨惰性B-NHL不同亚型与肝炎病毒感染的相关性。方法:回顾性分析中国医学科学院血液病医院1994年1月至2014年1月收治的733例初诊惰性B-NHL患者的肝炎病毒感染资料。与全国一般人群相对照,比较惰性B-NHL患者与全国一般人群肝炎病毒感染的差异。比较分析惰性B-NHL各亚型患者肝炎病毒感染的情况,并探讨其相关性。结果:733例惰性B-NHL患者乙肝表面抗原(hepatitis B surface antigen,HBs-Ag)阳性率为7.9%,与全国一般人群比较,差异无统计学意义(7.9%vs.7.2%,P=0.548)。在惰性B-NHL中,脾边缘区淋巴瘤(splenic marginal zone lymphoma,SMZL)48例,HBs-Ag阳性率为18.8%,明显高于全国一般人群(18.8%vs.7.2%,P=0.002)、其他惰性B-NHL(18.8%vs.7.2%,P=0.004)及其他边缘区淋巴瘤(marginal zone lymphoma,MZL)患者(18.8%vs.7.1%,P=0.005)。惰性B-NHL其他亚型患者HBs-Ag阳性率比较全国一般人群,差异均无统计学意义(P>0.05)。在HBs-Ag阳性患者中,乙肝"大三阳"在惰性B-NHL不同亚型中无显著性差异,但乙肝"小三阳"在SMZL组占16.7%,明显高于其他惰性B-NHL组(16.7%vs.4.7%,P<0.001)。惰性B-NHL患者抗丙型肝炎病毒抗体(hepatitis C virus antibody,HCV-Ab)阳性率为1.9%,较全国一般人群明显升高(1.9%vs.0.4%,P<0.001)。其中慢性淋巴细胞白血病(chronic lymphocytic leukemia,CLL)、淋巴浆细胞性淋巴瘤/华氏巨球蛋白血症(lymphoplasmacytic lymphoma/waldenstr?m macroglobulinemia,LPL/WM)、SMZL、毛细胞白血病(hairy cell leukemia,HCL)、结内边缘区淋巴瘤(nodal marginal zone B-cell lymphoma,NMZL)组患者抗HCV-Ab阳性率分别为2.2%、2.5%、4.2%、3.0%、3.7%均较全国一般人群明显升高(均P<0.05)。而慢性B淋巴细胞增殖性疾病不能分类(B-cell lymphoproliferative disorders,unclassified,B-LPD-U)、黏膜相关淋巴组织结外边缘区淋巴瘤(extranodal marginal zone B-cell lymphoma of mucosa-associated tissue lymphoma,MALT)、B-幼淋巴细胞白血病(B-cell prolymphocytic leukaemia,B-PLL)、滤泡性淋巴瘤(follicular lymphoma,FL)组与全国一般人群比较,差异均无统计学意义(均P>0.05)。结论:SMZL患者HBs-Ag阳性率明显高于全国一般人群及其他惰性B-NHL各亚型,提示HBV感染与我国SMZL的发生发展存在一定的相关性。

结内边缘区B细胞淋巴瘤临床病理观察

目的提高对结内边缘区B细胞淋巴瘤(NMZL)的认识。方法对1例结内NMZL进行临床、病理组织学和免疫组化观察,复习相关文献。结果患者男性,71岁,腹股沟淋巴结肿大起病。组织病变有突出的单核样B细胞增生和反滤泡结构,晚期呈弥漫性结节状和大细胞化,瘤细胞表达成熟B细胞免疫表型:CD20、CD79a(+),CD5、CD10和CD23(-),bcl-2(+)。历时6年,行23个疗程化疗,病情反复复发,终致累及全身淋巴结、骨髓和外周血。结论NMZL为少见的独立实体,原发于淋巴结的低度恶性B细胞淋巴瘤。临床表现为外周淋巴结肿大,惰性经过。

原发性皮肤边缘区B细胞淋巴瘤

报告1例原发性皮肤边缘区B细胞淋巴瘤(PCMZL)。患者男,26岁。右大腿伸侧、左肩部及左前臂各一红色或紫红色浸润性斑块,大小不等,界限清楚,表面可见米粒大丘疹,无鳞屑、破溃及压痛。皮损组织病理检查:真皮层可见淋巴样细胞弥漫或结节状浸润,少量累及表皮,浸润细胞中大量小至中等大小的中心细胞样淋巴细胞,胞质透亮,可见轻度核异形;表皮下、浸润细胞周围偶见浆细胞。免疫组化:可见大量反应性的CD3+T细胞,其周围环绕的小淋巴细胞CD20、CD79a及B细胞淋巴瘤/白血病因子(Bcl)-2均(+);肿瘤细胞增殖核抗原(Ki-67)(>40%+);浆细胞限制性表达轻链-λ,不表达轻链-κ;散在肿瘤细胞CD30、CD21、CD10、Bcl-6及D型细胞周期蛋白(cyclin D)1均(+)。诊断:PCMZL。治疗:予手术切除右大腿伸侧及左肩部皮损,术后随访至今,皮损未复发及未见新发皮损。

伴浆细胞分化的弥漫大B细胞淋巴瘤一例病例报告并文献复习

老年男性患者,以"腹股沟包块进行性肿大半年,肋骨疼痛2个月"为主诉入院,查体示脾大。既往贫血史30余年。入院化验示血清Ig M明显升高,血清免疫固定电泳示单克隆Ig M-κ阳性,外周血MYD88L265p突变阴性,骨髓涂片可见大量淋巴样浆细胞,骨髓免疫组化不除外脾边缘区淋巴瘤(SMZL)。后经淋巴结活检确诊为弥漫大B细胞淋巴瘤(DLBCL),经予CHOP方案化疗(环磷酰胺、吡柔比星、长春地辛、地塞米松)后取得部分缓解(PR)。

Fc受体样4蛋白在唾液腺黏膜相关淋巴组织结外边缘区B细胞淋巴瘤中的表达及意义

目的:通过检测唾液腺黏膜相关淋巴组织结外边缘区B细胞淋巴瘤(extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue B cell lymphoma,MALT淋巴瘤)中Fc受体样4(Fc receptor-like 4,FCRL4)蛋白的表达,分析其表达及分布特点与临床病理指标、预后等的相关性。方法:筛选2005—2013经病理确诊为唾液腺MALT淋巴瘤的病例作为实验组;以唇腺良性淋巴上皮病(benign lymphoepithelial lesions,BLEL)、大唾液腺BLEL及弥漫性大B细胞淋巴瘤(diffuse large B cell lymphoma,DLBCL)作为对照组。免疫组织化学(immunohistochemistry,IHC)法检测FCRL4蛋白表达。采用SPSS 17.0软件对FCRL4在实验组、对照组的表达及其与临床病理指标之间的关系进行分析,应用Kaplan-Meier法分析FCRL4表达与总体生存率之间的关系。结果:共收集到72例唾液腺MALT淋巴瘤。FCRL4表达主要定位于淋巴细胞的细胞膜和细胞浆,阳性细胞主要分布在上皮巢内及周边,且在唾液腺MALT淋巴瘤中的表达率显著高于唇腺BLEL(P=0.013)、大唾液腺BLEL(P=0.003)及DLBCL(P=0.001)。FCRL4蛋白表达与临床病理指标、总体生存率之间均无明显相关性(P>0.05)。结论:唾液腺MALT淋巴瘤中FCRL4主要表达于邻近上皮的淋巴细胞中,该类细胞可能与唾液腺MALT淋巴瘤的发生相关,可作为该肿瘤辅助诊断的指标。

边缘区B细胞淋巴瘤的临床和分子细胞遗传学研究进展

边缘区B细胞淋巴瘤 (MZBCL)是B细胞非霍奇金淋巴瘤中一种独特的亚型。近年来 ,在细胞和分子遗传学水平对MZBCL的发生发展机制的研究已有重要进展。MZBCL时 ,重排的VH基因亦是参与自身抗体产生的基因 ,提示该病源于自身反应性B细胞。多种染色体数量和结构异常及API2、BCL10和FAS等程序性死亡 (又称凋亡 )相关基因受累 ,表明程序性死亡受抑是MZBCL的主要发病原因。

肺原发性黏膜相关淋巴组织型边缘区B细胞淋巴瘤一例报告

本文报告1例肺原发性黏膜相关淋巴组织型边缘区B细胞淋巴瘤(PMZL-MALT)的病例。患者主因间断咳嗽咳痰4年,加重1年入院,给予抗感染治疗,效果不佳;实验室检查没有特异性指标,胸部强化CT检查显示肺实变。经气管镜检查取活检,病理诊断为PMZL-MALT。患者经过化疗,目前病情稳定并定期复查。

乳腺浸润性癌合并非霍奇金淋巴结内边缘区B细胞淋巴瘤6例临床病理分析

目的探讨乳腺浸润性癌合并非霍奇金淋巴结内边缘区B细胞淋巴瘤(non-Hodgkin lymph node inner marginal zone B cell lymphoma,NHLNMZL)的临床病理特征、诊断及鉴别诊断。方法采用免疫组化MaxVision法对6例乳腺浸润性癌合并NHLNMZL进行检测,并行21基因检测及NHLNMZL的基因检测。结果6例均为乳腺浸润性癌合并NHLNMZL,其中1例浸润性微乳头状癌有2枚淋巴结发生转移。淋巴瘤免疫表型:CD20弥漫阳性,CD21示FDC网扩大但较细,BCL-2、MNDA阳性。乳腺浸润性癌基因检测:其中4例表现为中危(RS=26.69),1例表现为高危(RS=34.21),1例表现为低危(RS=12.34);NHLNMZL中IgH、IgK、IgL阳性,FISH检测BCL-2、BCL-6、MYC均无重组。结论乳腺浸润性癌合并NHLNMZL虽属于恶性,但其侵袭性和恶性级别均较低,应与淋巴造血系统肿瘤鉴别。