CD30 is a CD40-inducible molecule that negatively regulates CD40-mediated immunoglobulin class switching in non-antigen-selected human B cells

被引：63

作者：

Cerutti, A

Schaffer, A

Shah, S

Zan, H

Liou, HC

Goodwin, RG

Casali, P ^{[1
]}

机构：

[1] Cornell Univ, Coll Med, Dept Pathol, Div Mol Immunol, New York, NY 10021 USA

[2] Cornell Univ, Grad Sch Med Sci, Program Immunol, New York, NY 10021 USA

[3] Cornell Univ, Coll Med, Dept Med, Div Immunol, New York, NY 10021 USA

[4] Immunex Corp, Seattle, WA 98101 USA

来源：

IMMUNITY | 1998年 / 9卷 / 02期

关键词：

D O I：

10.1016/S1074-7613(00)80607-X

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

We used our monoclonal model of germinal center maturation, CL-01 B cells, to investigate the role of CD30 in human B cell differentiation. CL-01 cells are IgM(+)IgD(+)CD30(+) and switch to IgG, IgA, and IgE when exposed to CD40L and IL-4. Switching is hampered by CD30 coengagement, possibly through interference with the CD40-mediated NF-kappa B-dependent transcriptional activation of downstream C-H genes. The physiological relevance of this phenomenon is emphasized by similar CD30-mediated effects in naive B cells. Expression of CD30 by these cells is induced by CD40L but is inhibited by B cell receptor coengagement and/or exposure to IL-6 and IL-12. Our data suggest that CD30 critically regulates the CD40-mediated differentiation of non-antigen-selected human B cells.

引用

页码：247 / 256

页数：10

共 46 条

[1] RETRACTED: Tumor necrosis factor receptor-associated factor (TRAF)-1, TRAF-2, and TRAF-3 interact in vivo with the CD30 cytoplasmic domain; TRAF-2 mediates CD30-induced nuclear factor kappa B activation (Retracted article. See vol 94, pg 12732, 1997) [J].

Ansieau, S ;

Scheffrahn, I ;

Mosialos, G ;

Brand, H ;

Duyster, J ;

Kaye, K ;

Harada, J ;

Dougall, B ;

Hubinger, G ;

Kieff, E ;

Herrmann, F ;

Leutz, A ;

Gruss, HJ .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (24) :14053-14058

[2] IDENTIFICATION OF A SOURCE OF BIOLOGICALLY-ACTIVE CD40 LIGAND [J].

ARMITAGE, RJ ;

SATO, TA ;

MACDUFF, BM ;

CLIFFORD, KN ;

ALPERT, AR ;

SMITH, CA ;

FANSLOW, WC .

EUROPEAN JOURNAL OF IMMUNOLOGY, 1992, 22 (08) :2071-2076

[3] THE CD40 LIGAND, GP39, IS DEFECTIVE IN ACTIVATED T-CELLS FROM PATIENTS WITH X-LINKED HYPER-IGM SYNDROME [J].

ARUFFO, A ;

FARRINGTON, M ;

HOLLENBAUGH, D ;

LI, X ;

MILATOVICH, A ;

NONOYAMA, S ;

BAJORATH, J ;

GROSMAIRE, LS ;

STENKAMP, R ;

NEUBAUER, M ;

ROBERTS, RL ;

NOELLE, RJ ;

LEDBETTER, JA ;

FRANCKE, U ;

OCHS, HD .

CELL, 1993, 72 (02) :291-300

[4]

Cerutti A, 1998, J IMMUNOL, V160, P2145

[5]

Choe JS, 1996, J IMMUNOL, V157, P1006

[6] HOW B-CELLS AND T-CELLS TALK TO EACH OTHER [J].

CLARK, EA ;

LEDBETTER, JA .

NATURE, 1994, 367 (6462) :425-428

[7] CD30-MEDIATED SIGNALING PROMOTES THE DEVELOPMENT OF HUMAN T-HELPER TYPE 2-LIKE T-CELLS [J].

DELPRETE, G ;

DECARLI, M ;

DELIOS, MM ;

DANIEL, KC ;

ALMERIGOGNA, F ;

ALDERSON, M ;

SMITH, CA ;

THOMAS, E ;

ROMAGNANI, S .

JOURNAL OF EXPERIMENTAL MEDICINE, 1995, 182 (06) :1655-1661

[8] CD30-dependent degradation of TRAF2: implications for negative regulation of TRAF signaling and the control of cell survival [J].

Duckett, CS ;

Thompson, CB .

GENES & DEVELOPMENT, 1997, 11 (21) :2810-2821

[9] MOLECULAR-CLONING AND EXPRESSION OF A NEW MEMBER OF THE NERVE GROWTH-FACTOR RECEPTOR FAMILY THAT IS CHARACTERISTIC FOR HODGKINS-DISEASE [J].

DURKOP, H ;

LATZA, U ;

HUMMEL, M ;

EITELBACH, F ;

SEED, B ;

STEIN, H .

CELL, 1992, 68 (03) :421-427

[10] A new protein containing an SH2 domain that inhibits JAK kinases [J].

Endo, TA ;

Masuhara, M ;

Yokouchi, M ;

Suzuki, R ;

Sakamoto, H ;

Mitsui, K ;

Matsumoto, A ;

Tanimura, S ;

Ohtsubo, M ;

Misawa, H ;

Miyazaki, T ;

Leonor, N ;

Taniguchi, T ;

Fujita, T ;

Kanakura, Y ;

Komiya, S ;

Yoshimura, A .

NATURE, 1997, 387 (6636) :921-924

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