日前,，IMIM（醫(yī)院德?tīng)栺R研究所）B細(xì)胞生物學(xué)研究小組聯(lián)合來(lái)自紐約西奈山的研究人員在Nature Immunol雜志發(fā)表論文"B cell–helper neutrophils stimulate the diversification and production of immunoglobulin in the marginal zone of the spleen"稱他們發(fā)現(xiàn)脾臟中也存在中性粒細(xì)胞,這是第一次發(fā)現(xiàn)中性粒細(xì)胞存在于脾臟內(nèi),且沒(méi)有被感染.,也發(fā)現(xiàn)這些中性粒細(xì)胞有可能具有免疫調(diào)節(jié)的作用.
中性粒細(xì)胞又稱所謂的清潔細(xì)胞,因?yàn)樗麄兪沁w移到感染和炎癥摧毀病原體地方的第一個(gè)細(xì)胞.到目前為止,科學(xué)文獻(xiàn)認(rèn)為中性粒細(xì)胞本質(zhì)上是卑微的合格士兵,僅僅限制感染的擴(kuò)張,作為第一個(gè)行動(dòng),為負(fù)責(zé)永久根除感染的免疫系統(tǒng)中的其他細(xì)胞鋪平道路.
該研究表明,在脾臟中發(fā)現(xiàn)的中性粒細(xì)胞沒(méi)有被感染,這在生物學(xué)領(lǐng)域是一項(xiàng)全新的知識(shí).
圖中,脾臟B淋巴細(xì)胞（藍(lán)色）被中性粒細(xì)胞（綠色）和內(nèi)皮細(xì)胞（紅色）環(huán)繞著.左側(cè)的圖像對(duì)應(yīng)一個(gè)正常的脾臟,右側(cè)是中性粒細(xì)胞減少癥患者的脾臟,他的中性粒細(xì)胞含量非常低.
研究人員注意到,中性粒細(xì)胞在脾臟的存在開(kāi)始于胎兒發(fā)育的時(shí)候,即使沒(méi)有傳染性過(guò)程的參與,這些在科學(xué)文獻(xiàn)里是未知的.這項(xiàng)研究擴(kuò)大到不同年齡的人群和其他哺乳動(dòng)物.均檢測(cè)到在脾臟中存在中性粒細(xì)胞,這表明這些中性粒細(xì)胞在脾臟中扮演著不同的角色.
脾臟中的中性粒細(xì)胞在B淋巴細(xì)胞的周圍,以幫助其激活,并在有病原體時(shí)提供第一快速反應(yīng).通過(guò)幾個(gè)不同的實(shí)驗(yàn)方法,我們已經(jīng)證明,脾臟中的中性粒細(xì)胞獲得與B細(xì)胞或B淋巴球相互作用的能力,誘導(dǎo)產(chǎn)生抗體,這種作用是在血液中的淋巴球循環(huán)不能做到的.
這一發(fā)現(xiàn)提高了我們對(duì)免疫系統(tǒng)保護(hù)我們免受感染機(jī)制的理解,必然要求所有更好的病理學(xué)控制和它聯(lián)系起來(lái).此外,當(dāng)面對(duì)某些疾病,如中性粒細(xì)胞減少癥（或中性粒細(xì)胞數(shù)量缺乏）時(shí),它不僅成為中性粒細(xì)胞缺乏癥的必要研究,而且這將影響抗體的產(chǎn)生.
這項(xiàng)工作為不同病原體感染的治療打開(kāi)了大門(mén),例如,開(kāi)發(fā)疫苗來(lái)增強(qiáng)脾臟中性粒細(xì)胞的能力,以便增加B淋巴細(xì)胞產(chǎn)生抗體的能力.（生物谷Bioon.com）
doi:10.1038/ni.2194
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PMID:
B cell–helper neutrophils stimulate the diversification and production of immunoglobulin in the marginal zone of the spleen
Irene Puga,Montserrat Cols,Carolina M Barra,Bing He,Linda Cassis,Maurizio Gentile,Laura Comerma,Alejo Chorny,Meimei Shan,Weifeng Xu,Giuliana Magri,Daniel M Knowles,Wayne Tam,April Chiu,James B Bussel,et al.
Neutrophils use immunoglobulins to clear antigen, but their role in immunoglobulin production is unknown. Here we identified neutrophils around the marginal zone (MZ) of the spleen, a B cell area specialized in T cell–independent immunoglobulin responses to circulating antigen. Neutrophils colonized peri-MZ areas after postnatal mucosal colonization by microbes and enhanced their B cell–helper function after receiving reprogramming signals, including interleukin 10 (IL-10), from splenic sinusoidal endothelial cells. Splenic neutrophils induced immunoglobulin class switching, somatic hypermutation and antibody production by activating MZ B cells through a mechanism that involved the cytokines BAFF, APRIL and IL-21. Neutropenic patients had fewer and hypomutated MZ B cells and a lower abundance of preimmune immunoglobulins to T cell–independent antigens, which indicates that neutrophils generate an innate layer of antimicrobial immunoglobulin defense by interacting with MZ B cells.
