On Wednesday, Oct. 31st, starting at Noon in CCSR 4205, Emily S. (Robinson Lab) will present:
Communicable ulcerative colitis induced by T-bet deficiency in the innate immune system
Wendy S. Garrett, Graham M. Lord, Shivesh Punit, Geanncarlo Lugo-Villarino, Sarkis K. Mazmanian, Susumu Ito, Jonathan N. Glickman, and Laurie H. Glimcher
Cell, Vol 131, 33-45, 05 October 2007
Link to article: click here
Tuesday, October 30, 2007
Monday, October 22, 2007
Oct. 24th (Wed)
On Wednesday, Oct. 24th, starting at Noon in CCSR 4205, Tin M. (Chen Lab) will present:
Regulation of the germinal center response by microRNA-155
Thai TH, Calado DP, Casola S, Ansel KM, Xiao C, Xue Y, Murphy A, Frendewey D, Valenzuela D, Kutok JL, Schmidt-Supprian M, Rajewsky N, Yancopoulos G, Rao A, Rajewsky K.
Science. 2007 Apr 27;316(5824):604-8.
Link to article: click here
and
Requirement of bic/microRNA-155 for normal immune function
Rodriguez A, Vigorito E, Clare S, Warren MV, Couttet P, Soond DR, van Dongen S, Grocock RJ, Das PP, Miska EA, Vetrie D, Okkenhaug K, Enright AJ, Dougan G, Turner M, Bradley A.
Science. 2007 Apr 27;316(5824):608-11.
Link to article: click here
-----
Tin's teaser:
MicroRNAs represent a fundamental layer of gene regulation that mediate posttranscriptional gene repression by binding to complementary mRNA transcripts of target genes. While small in stature, their impressions can be felt across various biological processes as computational prediction suggests that at least one-third of all protein-coding genes are regulated by miRNAs. Their role on the immune system was recently appreciated as two independent groups knocked out the gene that encodes for microRNA-155. T cells, B cells, and dendritic cells were all found to function improperly in these mutant mice and contributed to their immunodeficiency. Mir-155-deficient mice were unable to generate normal germinal center reactions, thereby impairing T cell-dependent antibody responses. These mutant mice also displayed significant lung airway remodeling that was consistent asthma pathology. Moreover, when vaccinated with an attenuated form of Samonella, the animals failed to develop protective immunity with the majority of mice succumbing to the virulent strain within a month. These observations suggest that miR-155 plays an important role in the homeostasis and function of the immune system. These studies also underscores the broad impact one particular microRNA can have by controlling multiple genes.
Regulation of the germinal center response by microRNA-155
Thai TH, Calado DP, Casola S, Ansel KM, Xiao C, Xue Y, Murphy A, Frendewey D, Valenzuela D, Kutok JL, Schmidt-Supprian M, Rajewsky N, Yancopoulos G, Rao A, Rajewsky K.
Science. 2007 Apr 27;316(5824):604-8.
Link to article: click here
and
Requirement of bic/microRNA-155 for normal immune function
Rodriguez A, Vigorito E, Clare S, Warren MV, Couttet P, Soond DR, van Dongen S, Grocock RJ, Das PP, Miska EA, Vetrie D, Okkenhaug K, Enright AJ, Dougan G, Turner M, Bradley A.
Science. 2007 Apr 27;316(5824):608-11.
Link to article: click here
-----
Tin's teaser:
MicroRNAs represent a fundamental layer of gene regulation that mediate posttranscriptional gene repression by binding to complementary mRNA transcripts of target genes. While small in stature, their impressions can be felt across various biological processes as computational prediction suggests that at least one-third of all protein-coding genes are regulated by miRNAs. Their role on the immune system was recently appreciated as two independent groups knocked out the gene that encodes for microRNA-155. T cells, B cells, and dendritic cells were all found to function improperly in these mutant mice and contributed to their immunodeficiency. Mir-155-deficient mice were unable to generate normal germinal center reactions, thereby impairing T cell-dependent antibody responses. These mutant mice also displayed significant lung airway remodeling that was consistent asthma pathology. Moreover, when vaccinated with an attenuated form of Samonella, the animals failed to develop protective immunity with the majority of mice succumbing to the virulent strain within a month. These observations suggest that miR-155 plays an important role in the homeostasis and function of the immune system. These studies also underscores the broad impact one particular microRNA can have by controlling multiple genes.
Tuesday, October 16, 2007
Oct. 17th (Wed)
On Wednesday, Oct. 17th, starting at Noon in CCSR 4205, Ana da S. (Fathman Lab) will present:
Dynamic imaging of chemokine-dependent CD8+ T cell help for CD8+ T cell responses
Stéphanie Hugues, Alix Scholer, Alexandre Boissonnas, Alexander Nussbaum, Christophe Combadière, Sebastian Amigorena & Luc Fetle
Nature Immunology 8, 921 - 930 (2007)
Link to article: click here
-----
Ana's teaser:
Interaction between cells during an immune response is one of the mechanisms that often increases the efficiency in eliminating target antigens. It is well established that CD4+ T cells are the major “helper” cell for B and CD8 T cell activation, by releasing cytokines that directly activate these cells or by increasing the ability of APCs to professionally activate other CD4+ or CD8+ T cells (ex. increasing the expression of co-stimulators molecules). Similar to CD4+ T cells, NK cells and NK T cells seem to influence the maturation of DCs and “help” CD4+ and CD8+ T cell responses in vitro and in vivo. We have been mainly focused on enhancing the immune response to a specific antigen by increasing function of the “helper” cells specific to the same antigen and underscoring the effect of bystanders cells that somehow are also activated in these microenvironments. Here Hugues et al. beautifully show during the initiation of antigen-specific CD8+ T cells that naïve polyclonal CD8+ T cells also interact with the mature dendritic cells and as a result a strong CD8+ T cell antigen-specific response is elaborated. The interaction between DCs and poly-T cells seem to be dependent on CCR5 chemokine. Then, the strong CD8+ T cell response induced by mature DCs against a first peptide favored the induction of a second antigen-specific CD8+ T cell strong enough to mediate rejection of an established B16 tumor.
Dynamic imaging of chemokine-dependent CD8+ T cell help for CD8+ T cell responses
Stéphanie Hugues, Alix Scholer, Alexandre Boissonnas, Alexander Nussbaum, Christophe Combadière, Sebastian Amigorena & Luc Fetle
Nature Immunology 8, 921 - 930 (2007)
Link to article: click here
-----
Ana's teaser:
Interaction between cells during an immune response is one of the mechanisms that often increases the efficiency in eliminating target antigens. It is well established that CD4+ T cells are the major “helper” cell for B and CD8 T cell activation, by releasing cytokines that directly activate these cells or by increasing the ability of APCs to professionally activate other CD4+ or CD8+ T cells (ex. increasing the expression of co-stimulators molecules). Similar to CD4+ T cells, NK cells and NK T cells seem to influence the maturation of DCs and “help” CD4+ and CD8+ T cell responses in vitro and in vivo. We have been mainly focused on enhancing the immune response to a specific antigen by increasing function of the “helper” cells specific to the same antigen and underscoring the effect of bystanders cells that somehow are also activated in these microenvironments. Here Hugues et al. beautifully show during the initiation of antigen-specific CD8+ T cells that naïve polyclonal CD8+ T cells also interact with the mature dendritic cells and as a result a strong CD8+ T cell antigen-specific response is elaborated. The interaction between DCs and poly-T cells seem to be dependent on CCR5 chemokine. Then, the strong CD8+ T cell response induced by mature DCs against a first peptide favored the induction of a second antigen-specific CD8+ T cell strong enough to mediate rejection of an established B16 tumor.
Monday, October 8, 2007
Oct. 10th (Wed)
On Wednesday, Oct. 10th, starting at Noon in CCSR 4205, Candace C. (McDevitt and Utz Labs) will present:
Mammalian N-Glycan Branching Protects against Innate Immune Self-Recognition and Inflammation in Autoimmune Disease Pathogenesis
Ryan S. Green, Erica L. Stone, Mari Tenno, Eero Lehtonen, Marilyn G. Farquhar and Jamey D. Marth
Immunity, Volume 27, Issue 2, Pages 308-320
Link to article: click here
-----
Candace's teaser:
Glycosylation plays a critical role in the regulation of numerous cellular processes, including cell adhesion, cell activation, and protein trafficking. One of the enzymes responsible for a specific glycan is alpha-mannosidase II. Interestingly, when this gene is knocked out in mice, they develop an autoimmune disease similar to lupus! In addition, the manifestation of disease is not dependent on adaptive immunity. These findings underscore the significance of sugar moieties as antigens. It also suggests that altered sugars can act as pathogen-associated molecular patterns (PAMPs) and trigger an immune response.
Mammalian N-Glycan Branching Protects against Innate Immune Self-Recognition and Inflammation in Autoimmune Disease Pathogenesis
Ryan S. Green, Erica L. Stone, Mari Tenno, Eero Lehtonen, Marilyn G. Farquhar and Jamey D. Marth
Immunity, Volume 27, Issue 2, Pages 308-320
Link to article: click here
-----
Candace's teaser:
Glycosylation plays a critical role in the regulation of numerous cellular processes, including cell adhesion, cell activation, and protein trafficking. One of the enzymes responsible for a specific glycan is alpha-mannosidase II. Interestingly, when this gene is knocked out in mice, they develop an autoimmune disease similar to lupus! In addition, the manifestation of disease is not dependent on adaptive immunity. These findings underscore the significance of sugar moieties as antigens. It also suggests that altered sugars can act as pathogen-associated molecular patterns (PAMPs) and trigger an immune response.
Monday, October 1, 2007
Oct. 3rd (Wed)
On Wednesday, Oct. 3rd, starting at Noon in CCSR 4205, Byron E. (Nolan Lab) will present:
"A Statistician Visits the Flow Lab"
Description:
Statisticians are just now really discovering flow cytometry,
particularly phospho-flow cytometry, as a rich source of high
throughput data. In this talk, I will discuss the problem of analyzing
flow data, in the context of some experiments being done in the Nolan
lab, from a statistician's point-of-view, some pointers to the current
state-of-the-art (published and not), and a glimpse at the tools some
of us have been building to help bring more collaborators and
analytical options to the table.
"A Statistician Visits the Flow Lab"
Description:
Statisticians are just now really discovering flow cytometry,
particularly phospho-flow cytometry, as a rich source of high
throughput data. In this talk, I will discuss the problem of analyzing
flow data, in the context of some experiments being done in the Nolan
lab, from a statistician's point-of-view, some pointers to the current
state-of-the-art (published and not), and a glimpse at the tools some
of us have been building to help bring more collaborators and
analytical options to the table.
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