Major histocompatibility complex class II hyperexpression on B cells in interleukin 4-transgenic mice does not lead to B cell proliferation and hypergammaglobulinemia

1991 ◽  
Vol 21 (4) ◽  
pp. 921-925 ◽  
Author(s):  
Werner Müller ◽  
Ralf Kühn ◽  
Klaus Rajewsky
Keyword(s):  
Cell Proliferation ◽  
Major Histocompatibility Complex ◽  
B Cells ◽  
Transgenic Mice ◽  
Major Histocompatibility Complex Class ◽  
B Cell ◽  
Class Ii ◽  
Interleukin 4 ◽  
Complex Class ◽  
Histocompatibility Complex

B-cell control region at the 5' end of a major histocompatibility complex class II gene: sequences and factors

1988 ◽  
Vol 8 (10) ◽  
pp. 3975-3987
Author(s):  
A Dorn ◽  
H J Fehling ◽  
W Koch ◽  
M Le Meur ◽  
P Gerlinger ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
B Cells ◽  
Major Histocompatibility Complex Class ◽  
B Cell ◽  
Simian Virus 40 ◽  
Class Ii ◽  
Immunoglobulin Gene ◽  
Complex Class ◽  
Major Histocompatibility ◽  
Histocompatibility Complex

Transcription of major histocompatibility complex class II genes is elaborately regulated. Mouse class II genes are transcribed primarily in B cells, peripheral macrophages and interdigitating cells, and thymic cortical and medullary cells. In this study, we began to identify the DNA sequences and protein factors that control expression of a class II gene in B cells, addressing in particular how closely they resemble those that regulate immunoglobulin gene expression. We describe a region upstream of the E alpha gene that is crucial for its transcription in the B cells of transgenic mice but is less important in cultured B-cell lines. The sequence of this region reveals several familiar motifs, including a second X-Y pair reminiscent of that residing in the promoter-proximal region of all class II genes, a B motif strikingly homologous to that associated with the immunoglobulin kappa gene enhancer, several Ephrussi motifs, and a Pu box-like sequence very similar to that implicated in simian virus 40 and lymphotrophic papovavirus expression in B cells. Careful study of the proteins that bind specifically to these different motifs prompts us to suggest that major histocompatibility complex class II and immunoglobulin genes rely on quite different factors to achieve B-cell-specific expression.

scholarly journals B-cell control region at the 5' end of a major histocompatibility complex class II gene: sequences and factors.

1988 ◽  
Vol 8 (10) ◽  
pp. 3975-3987 ◽  
Author(s):  
A Dorn ◽  
H J Fehling ◽  
W Koch ◽  
M Le Meur ◽  
P Gerlinger ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
B Cells ◽  
Major Histocompatibility Complex Class ◽  
B Cell ◽  
Simian Virus 40 ◽  
Class Ii ◽  
Immunoglobulin Gene ◽  
Complex Class ◽  
Major Histocompatibility ◽  
Histocompatibility Complex

Transcription of major histocompatibility complex class II genes is elaborately regulated. Mouse class II genes are transcribed primarily in B cells, peripheral macrophages and interdigitating cells, and thymic cortical and medullary cells. In this study, we began to identify the DNA sequences and protein factors that control expression of a class II gene in B cells, addressing in particular how closely they resemble those that regulate immunoglobulin gene expression. We describe a region upstream of the E alpha gene that is crucial for its transcription in the B cells of transgenic mice but is less important in cultured B-cell lines. The sequence of this region reveals several familiar motifs, including a second X-Y pair reminiscent of that residing in the promoter-proximal region of all class II genes, a B motif strikingly homologous to that associated with the immunoglobulin kappa gene enhancer, several Ephrussi motifs, and a Pu box-like sequence very similar to that implicated in simian virus 40 and lymphotrophic papovavirus expression in B cells. Careful study of the proteins that bind specifically to these different motifs prompts us to suggest that major histocompatibility complex class II and immunoglobulin genes rely on quite different factors to achieve B-cell-specific expression.

scholarly journals Complex architecture of major histocompatibility complex class II promoters: reiterated motifs and conserved protein-protein interactions.

1996 ◽  
Vol 16 (9) ◽  
pp. 4683-4690 ◽  
Author(s):  
N Jabrane-Ferrat ◽  
J D Fontes ◽  
J M Boss ◽  
B M Peterlin
Keyword(s):  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Class ◽  
B Cell ◽  
Interferon Gamma ◽  
Class Ii ◽  
Inducible Expression ◽  
Complex Class ◽  
Major Histocompatibility ◽  
Flanking Sequence ◽  
Histocompatibility Complex

The S box (also known as at the H, W, or Z box) is the 5'-most element of the conserved upstream sequences in promoters of major histocompatibility complex class II genes. It is important for their B-cell-specific and interferon gamma-inducible expression. In this study, we demonstrate that the S box represents a duplication of the downstream X box. First, RFX, which is composed of the RFX5-p36 heterodimer that binds to the X box, also binds to the S box and its 5'-flanking sequence. Second, NF-Y, which binds to the Y box and increases interactions between RFX and the X box, also increases the binding of RFX to the S box. Third, RFXs bound to S and X boxes interact with each other in a spatially constrained manner. Finally, we confirmed these protein-protein and protein-DNA interactions by expressing a hybrid RFX5-VP16 protein in cells. We conclude that RFX binds to S and X boxes and that complex interactions between RFX and NF-Y direct B-cell-specific and interferon gamma-inducible expression or major histocompatibility complex class II genes.

scholarly journals Follicular dendritic cells help resting B cells to become effective antigen-presenting cells: induction of B7/BB1 and upregulation of major histocompatibility complex class II molecules.

1993 ◽  
Vol 178 (6) ◽  
pp. 2055-2066 ◽  
Author(s):  
M H Kosco-Vilbois ◽  
D Gray ◽  
D Scheidegger ◽  
M Julius
Keyword(s):  
Dendritic Cells ◽  
Major Histocompatibility Complex ◽  
B Cells ◽  
Major Histocompatibility Complex Class ◽  
B Cell ◽  
Antigen Presenting Cells ◽  
Follicular Dendritic Cells ◽  
Complex Class ◽  
Histocompatibility Complex ◽  
Antigen Presenting

This study was designed to investigate whether follicular dendritic cells (FDC) can activate B cells to a state in which they can function as effective antigen-presenting cells (APC). High buoyant density (i.e., resting) B cells specific for 2,4-dinitro-fluorobenzene (DNP) were incubated with DNP-ovalbumin (OVA) bearing FDC, after which their capacity to process and present to an OVA-specific T cell clone was assessed. The efficacies of alternative sources of antigen and activation signals in the induction of B cell APC function were compared with those provided by FDC. Only FDC and Sepharose beads coated with anti-immunoglobulin (Ig)kappa monoclonal antibody provided the necessary stimulus. FDC carrying inappropriate antigens also induced B cell APC function in the presence of exogenous DNP-OVA. However, in circumstances where soluble DNP-OVA was limiting, FDC bearing complexes containing DNP, which could crosslink B cell Ig receptors, induced the most potent APC function. Analysis by flow cytometry revealed that within 24 h of coculture with FDC, a significant percentage of B cells increased in size and expressed higher levels of major histocompatibility complex class II. By 48 h, an upregulation of the costimulatory molecule, B7/BB1, occurred, but only when exposed to the FDC bearing DNP. Taken together, the results demonstrate that FDC have the capacity to activate resting B cells to a state in which they can function as APC for T cells. The stimuli that FDC provide may include: (a) an antigen-dependent signal that influences the upregulation of B7/BB1; and (b) possibly a signal independent of crosslinking mIg that results in Ig internalization. The relevance of these findings to the formation of germinal centers and maintenance of the humoral response is discussed.

scholarly journals Major histocompatibility complex class II molecules induce the formation of endocytic MIIC-like structures.

1994 ◽  
Vol 126 (4) ◽  
pp. 967-977 ◽  
Author(s):  
J Calafat ◽  
M Nijenhuis ◽  
H Janssen ◽  
A Tulp ◽  
S Dusseljee ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
B Cells ◽  
Major Histocompatibility Complex Class ◽  
Class Ii ◽  
Kidney Cells ◽  
Complex Class ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Endocytic Compartments ◽  
Lysosomal Proteins

During biosynthesis, major histochompatibility complex class II molecules are transported to the cell surface through a late endocytic multilaminar structure with lysosomal characteristics. This structure did not resemble any of the previously described endosomal compartments and was termed MIIC. We show here that continuous protein synthesis is required for the maintenance of MIIC in B cells. Transfection of class II molecules in human embryonal kidney cells induces the formation of multilaminar endocytic structures that are morphologically analogous to MIIC in B cells. Two lysosomal proteins (CD63 and lamp-1), which are expressed in MIIC of B cells, are also present in the structures induced by expression of major histocompatibility complex class II molecules. Moreover, endocytosed HRP enters the induced structures defining them as endocytic compartments. Exchanging the transmembrane and cytoplasmic tail of the class II alpha and beta chains for that of HLA-B27 does not result in the induction of multilaminar structures, and the chimeric class II molecules are now located in multivesicular structures. This suggests that expression of class II molecules is sufficient to induce the formation of characteristic MIIC-like multilaminar structures.

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