Gut-associated lymphoid tissue contains the molecular machinery to support T-cell-dependent and T-cell-independent class switch recombination

被引:66
作者
Barone, F. [1 ]
Patel, P. [1 ,2 ]
Sanderson, J. D. [2 ]
Spencer, J. [1 ]
机构
[1] Kings Coll London, Peter Gorer Dept Immunobiol, London WC2R 2LS, England
[2] Kings Coll London, Div Nutr Sci, London WC2R 2LS, England
基金
英国生物技术与生命科学研究理事会;
关键词
INDUCED CYTIDINE DEAMINASE; IGA-PRODUCING CELLS; LAMINA PROPRIA; B-CELLS; APRIL; EXPRESSION; RECEPTORS; BAFF; DIFFERENTIATION; MUCOSAL;
D O I
10.1038/mi.2009.106
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
A PRoliferation-Inducing Ligand (APRIL) is a secreted cytokine member of the tumor necrosis factor family. It is a B-cell survival factor that also induces class switch recombination (CSR) toward immunoglobulin A (IgA), independent of T cells. It is therefore an important contributor to the maintenance of the mucosal immunological barrier, which has been linked to a putative extrafollicular inductive phase of the IgA response in lamina propria. By immunohistochemistry (IHC) and quantitative real-time PCR (qRT-PCR) on microdissected tissue from normal human gut, we observed APRIL expression, together with TACI (transmembrane activator and CAML interactor) and BCMA (B-cell maturation antigen), in gut-associated lymphoid tissue (GALT), lamina propria, and in the epithelium of stomach, small and large intestine, and rectum. However, no activation-induced cytidine deaminase (AID) expression (an absolute requirement for class switching) was detected in lamina propria by IHC or qRT-PCR. APRIL and its receptors were only observed alongside AID in GALT, showing that GALT contains the apparatus to support both T-independent and T-dependent routes to IgA CSR.
引用
收藏
页码:495 / 503
页数:9
相关论文
共 26 条
[1]
Cutting edge: The dependence of plasma cells and independence of memory B cells on BAFF and APRIL [J].
Benson, Micah J. ;
Dillon, Stacey R. ;
Castigli, Emanuela ;
Geha, Raif S. ;
Xu, Shengli ;
Lam, Konk-Peng ;
Noelle, Randolph J. .
JOURNAL OF IMMUNOLOGY, 2008, 180 (06) :3655-3659
[2]
Gut IgA class switch recombination in the absence of CD40 does not occur in the lamina propria and is independent of germinal centers [J].
Bergqvist, Peter ;
Gardby, Eva ;
Stensson, Anneli ;
Bemark, Mats ;
Lycke, Nils Y. .
JOURNAL OF IMMUNOLOGY, 2006, 177 (11) :7772-7783
[3]
BJERKE K, 1986, CLIN EXP IMMUNOL, V64, P432
[4]
Activation-induced cytidine deaminase expression in follicular dendritic cell networks and interfollicular large B cells supports functionality of ectopic lymphoid neogenesis in autoimmune sialoadenitis and MALT lymphoma in Sjogren's syndrome [J].
Bombardieri, Michele ;
Barone, Francesca ;
Humby, Frances ;
Kelly, Stephen ;
McGurk, Mark ;
Morgan, Peter ;
Challacombe, Stephen ;
De Vita, Salvatore ;
Valesini, Guido ;
Spencer, Jo ;
Pitzalis, Costantino .
JOURNAL OF IMMUNOLOGY, 2007, 179 (07) :4929-4938
[5]
BAFF, APRIL and their receptors: Structure, function and signaling [J].
Bossen, Claudia ;
Schneider, Pascal .
SEMINARS IN IMMUNOLOGY, 2006, 18 (05) :263-275
[6]
Human intestinal IgA response is generated in the organized gut-associated lymphoid tissue but not in the lamina propria [J].
Boursier, L ;
Gordon, JN ;
Thiagamoorthy, S ;
Edgeworth, JD ;
Spencer, J .
GASTROENTEROLOGY, 2005, 128 (07) :1879-1889
[7]
From B to A the mucosal way [J].
Brandtzaeg, P ;
Baekkevold, ES ;
Morton, HC .
NATURE IMMUNOLOGY, 2001, 2 (12) :1093-1094
[8]
Peripheral development of B cells in mouse and man [J].
Carsetti, R ;
Rosado, MM ;
Wardemann, H .
IMMUNOLOGICAL REVIEWS, 2004, 197 :179-191
[9]
Impaired IgA class switching in APRIL-deficient mice [J].
Castigli, E ;
Scott, S ;
Dedeoglu, F ;
Bryce, P ;
Jabara, H ;
Bhan, AK ;
Mizoguchi, E ;
Geha, RS .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2004, 101 (11) :3903-3908
[10]
Regulated expression of BAFF-binding receptors during human B cell differentiation [J].
Darce, Jaime R. ;
Arendt, Bonnie K. ;
Wu, Xiaosheng ;
Jelinek, Diane F. .
JOURNAL OF IMMUNOLOGY, 2007, 179 (11) :7276-7286