B-1 cells express transgelin 2:: Unexpected lymphocyte expression of a smooth muscle protein identified by proteomic analysis of peritoneal B-1 cells

被引:20
作者
Frances, Ruben
Tumang, Joseph R.
Kaku, Hiroaki
Gurdak, Sean M.
Rothstein, Thomas L. [1 ]
机构
[1] Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA
[2] Boston Univ, Sch Med, Dept Microbiol, Boston, MA 02118 USA
[3] Boston Univ, Med Ctr, Evans Mem Dept Clin Res, Immunobiol Unit, Boston, MA 02118 USA
关键词
B cells; proteomics; rodent; SM22B;
D O I
10.1016/j.molimm.2005.12.011
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
B-1 cells constitute a unique B cell subset that differs phenotypically, biochemically, and functionally from the predominant population of conventional B-2 cells. Functional differences include constitutive secretion of natural immunoglobulin and failure of BCR signaling to initiate proliferation. The origin of these differences remains uncertain. We hypothesized that unbiased analysis of differences in protein expression between highly pure populations of B-1 and B-2 cells might provide information not readily available through other means. To pursue this, we undertook 2D gel analysis of B-1 and B-2 cells combined with mass spectrometry. We identified the smooth muscle protein, transgelin 2, in peritoneal (but not splenic) B-1 cells and did not find it in splenic B-2 cells; these results were confirmed by Western blot analysis, which showed a more than 60-fold difference in transgelin 2 expression between peritoneal B-1 and splenic B-2 cells. In contrast, levels of transgelin 2 RNA differed to a much lesser extent (3-fold) in the two B cell populations, so transgelin 2 is an example of a molecule whose subset-specific expression is more readily detected by proteomic than transcriptomic analyses. Finally, transgelin 2 protein expression was induced in splenic B-2 cells; thus, transgelin 2 joins a number of other inducible molecules that are constitutively expressed by peritoneal B-1 but not splenic B-2 cells. Although the role of transgelin 2 in B-1 cell function remains uncertain, identification of this molecule demonstrates the value of examining protein expression in this B cell subset. (c) 2006 Elsevier Ltd. All rights reserved.
引用
收藏
页码:2124 / 2129
页数:6
相关论文
共 35 条
[11]   Splenic and peritoneal B-1 cells differ in terms of transcriptional and proliferative features that separate peritoneal B-1 from splenic B-2 cells [J].
Fischer, GM ;
Solt, LA ;
Hastings, WD ;
Yang, KJ ;
Gerstein, RM ;
Nikolajczyk, BS ;
Clarke, SH ;
Rothstein, TL .
CELLULAR IMMUNOLOGY, 2001, 213 (01) :62-71
[12]   Cutting edge:: B-1 cells are deficient in Lck:: Defective B cell receptor signal transduction in B-1 cells occurs in the absence of elevated Lck expression [J].
Francés, R ;
Tumang, JR ;
Rothstein, TL .
JOURNAL OF IMMUNOLOGY, 2005, 175 (01) :27-31
[13]   INDUCTION OF THE TRANSCRIPTION FACTORS NF-KB, AP-1 AND NF-AT DURING B-CELL STIMULATION THROUGH THE CD40 RECEPTOR [J].
FRANCIS, DA ;
KARRAS, JG ;
KE, XY ;
SEN, R ;
ROTHSTEIN, TL .
INTERNATIONAL IMMUNOLOGY, 1995, 7 (02) :151-161
[14]   Actin depolymerization transduces the strength of B-cell receptor stimulation [J].
Hao, SL ;
August, A .
MOLECULAR BIOLOGY OF THE CELL, 2005, 16 (05) :2275-2284
[15]   B cell development pathways [J].
Hardy, RR ;
Hayakawa, K .
ANNUAL REVIEW OF IMMUNOLOGY, 2001, 19 :595-621
[16]  
HARTWIG JH, 1995, J IMMUNOL, V155, P3769
[17]   B-1 cells: the lineage question revisited [J].
Herzenberg, LA .
IMMUNOLOGICAL REVIEWS, 2000, 175 :9-22
[18]  
Jugloff LS, 1997, J IMMUNOL, V159, P1096
[19]   Signal transducer and activator of transcription-3 (STAT3) is constitutively activated in normal, self-renewing B-1 cells but only inducibly expressed in conventional B lymphocytes [J].
Karras, JG ;
Wang, ZH ;
Huo, L ;
Howard, RG ;
Frank, DA ;
Rothstein, TL .
JOURNAL OF EXPERIMENTAL MEDICINE, 1997, 185 (06) :1035-1042
[20]   Antibody repertoire and gene expression profile: Implications for different developmental and functional traits of splenic and peritoneal B-1 lymphocytes [J].
Kretschmer, K ;
Jungebloud, A ;
Stopkowicz, J ;
Stoermann, B ;
Hoffmann, R ;
Weiss, S .
JOURNAL OF IMMUNOLOGY, 2003, 171 (03) :1192-1201