Multitasking of Ig-α and Ig-β to Regulate B Cell Antigen Receptor Function

Wienands, Jürgen; Engels, Niklas

doi:10.3109/08830180109045585

Cited by 21 publications

(13 citation statements)

References 109 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Figure 3 confirms that membrane-bound antigen (J558L[mHEL]) also cannot activate IgM/b Y AE L . Note that activation is also severely compromised (though not impossible) in IgM/b B cells, which is in agreement with experiments that report an important role for Iga in B cell activation [38]. …”

Section: Active Transport Processes Are Involved In Membrane Antigen supporting

confidence: 70%

Formation of the B cell synapse: retention or recruitment?

Iber

2005

CMLS, Cell. Mol. Life Sci.

View full text Add to dashboard Cite

Interaction of B cells with membrane antigen results in the formation of the B cell synapse: the B cell receptor (BCR) and antigen concentrate in the contact zone while CD45/B220 and the phosphatase SHP-1 are excluded. This study shows that, unlike in T cells, synapse formation does not require active transport processes (while subsequent antigen extraction and IgM downregulation do). The synapse architecture depends on the available protein ligands in the contact zone. Thus Syk, IgM and Fc receptor accumulation require the presence of ITAM-bearing BCRs, membrane antigen and membrane (IgG-containing) immune complexes, respectively. Remarkably, non-bound proteins are frequently not only homogeneously distributed but excluded from the contact zone. These results suggest that proteins mainly reach the contact zone by undirected diffusion, and in order not to be expelled by molecular crowding they require capture by and fixation to a binding protein.

show abstract

Section: Active Transport Processes Are Involved In Membrane Antigen supporting

confidence: 70%

Formation of the B cell synapse: retention or recruitment?

Iber

2005

CMLS, Cell. Mol. Life Sci.

View full text Add to dashboard Cite

show abstract

“…This gene encodes the Igα (CD79a) molecule, which along with Igβ (CD79b) is an essential component of the B cell receptor (BCR). Igα and Igβ are responsible for the cell surface expression of the BCR, BCR signaling, and trafficking of the antigen/BCR complex to appropriate compartments for antigen processing and peptide loading of MHC class II [188]. These events are necessary for the recognition and presentation of antigen by B cells.…”

Section: Ets1mentioning

confidence: 99%

ETS transcription factors and regulation of immunity

Gallant

Gilkeson

2006

Arch. Immunol. Ther. Exp.

151

122

View full text Add to dashboard Cite

The ETS family is a diverse group of transcription factors that control the expressions of genes that participate in an array of cellular activities, ranging from mitosis to apoptosis. As a consequence of regulating these processes, most ETS factors are oncogenic. However, there is growing evidence that ETS factors are also essential to regulation of the immune system. Of the 29 recognized ETS factors, nine are known to regulate genes involved in immunity, including Ets1, Ets2, GABP, Fli1, Elf1, MEF, ESE1, PU.1, and SpiB. These ETS factors typically activate the transcription of genes associated with pathogen and tumor defense, but several also demonstrate ability to repress transcription. Ets1 and PU.1 appear to have the greatest impact on immunity, primarily through their control of immune cell development. Alterations of Fli1 and Elf1 expression are associated with autoimmunity, emphasizing the role of ETS factors as not only positive, but also negative regulators of immunity. This review summarizes the roles of ETS factors in development of the immune system, defense against pathogens and malignancies, and self-tolerance.

show abstract

“…Wienands et al . (49) recently suggested that the Igα monophosphorylated ITAM functions as an immunoreceptor tyrosine‐based inhibitory motif (ITIM) leading to the recruitment of such negative regulators as SH2 domain‐containing phosphatase‐1 (SHP‐1), which limit BCR signaling by dephosphorylating‐activated src family kinases and SLP‐65.…”

Section: Distinct Functions Of Igα and Igβin Vivo May Correlate With mentioning

confidence: 99%

The avian B‐cell receptor complex: distinct roles of Igα and Igβ in B‐cell development

Pike

Baig

Ratcliffe

2004

Immunological Reviews

View full text Add to dashboard Cite

The bursa of Fabricius has evolved in birds as a gut-associated site of B-cell lymphopoiesis that is segregated from the development of other hematopoietic lineages. Despite differences in the developmental progression of chicken as compared to murine B-cell lymphopoiesis, cell-surface immunoglobulin (sIg) expression has been conserved in birds as an essential checkpoint in B-cell development. B-cell precursors that express an sIg complex that includes the evolutionarily conserved Igalpha/beta heterodimer colonize lymphoid follicles in the bursa, whereas B-cell precursors that fail to express sIg due to non-productive V(D)J recombination are eliminated. Productive retroviral gene transfer has allowed us to introduce chimeric receptor constructs into developing B-cell precursors in vivo. Chimeric proteins comprising the extracellular and transmembrane regions of murine CD8alpha fused to the cytoplasmic domain of chicken Igalpha efficiently supported B-cell development in precursors that lacked endogenous sIg expression. By contrast, expression of an equivalent chimeric receptor containing the cytoplasmic domain of Igbeta actively inhibited B-cell development. Consequently, the cytoplasmic domains of Igalpha and Igbeta play functionally distinct roles in chicken B-cell development.

show abstract

Multitasking of Ig-α and Ig-β to Regulate B Cell Antigen Receptor Function

Cited by 21 publications

References 109 publications

Formation of the B cell synapse: retention or recruitment?

Formation of the B cell synapse: retention or recruitment?

ETS transcription factors and regulation of immunity

The avian B‐cell receptor complex: distinct roles of Igα and Igβ in B‐cell development

Contact Info

Product

Resources

About