Orchestrating B cell lymphopoiesis through interplay of IL-7 receptor and pre-B cell receptor signalling

被引:245
作者
Clark, Marcus R. [1 ,2 ]
Mandal, Malay [1 ,2 ]
Ochiai, Kyoko [3 ]
Singh, Harinder [4 ]
机构
[1] Univ Chicago, Rheumatol Sect, Chicago, IL 60637 USA
[2] Univ Chicago, Gwen Knapp Ctr Lupus & Immunol Res, Chicago, IL 60637 USA
[3] Tohoku Univ Grad, Sch Med, Dept Biochem, Sendai, Miyagi, Japan
[4] Genentech Inc, Dept Discovery Immunol, Redwood City, CA USA
关键词
IMMUNOGLOBULIN HEAVY-CHAIN; SEVERE COMBINED IMMUNODEFICIENCY; REGULATES V(D)J RECOMBINATION; TRANSCRIPTION FACTOR EBF; ADAPTER PROTEIN SLP-65; ABL TYROSINE KINASE; BONE-MARROW; LYMPHOCYTE DEVELOPMENT; ANTIGEN-RECEPTOR; DEFICIENT MICE;
D O I
10.1038/nri3570
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
The development of B cells is dependent on the sequential DNA rearrangement of immunoglobulin loci that encode subunits of the B cell receptor. The pathway navigates a crucial checkpoint that ensures expression of a signalling-competent immunoglobulin heavy chain before commitment to rearrangement and expression of an immunoglobulin light chain. The checkpoint segregates proliferation of pre-B cells from immunoglobulin light chain recombination and their differentiation into B cells. Recent advances have revealed the molecular circuitry that controls two rival signalling systems, namely the interleukin-7 (IL-7) receptor and the pre-B cell receptor, to ensure that proliferation and immunoglobulin recombination are mutually exclusive, thereby maintaining genomic integrity during B cell development.
引用
收藏
页码:69 / 80
页数:12
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