Talk:2016 Group 3 Project

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Revision as of 10:55, 10 May 2016 by Z3463953 (talk | contribs)
2016 Projects: Group 1 | Group 2 | Group 3 | Group 4 | Group 5 | Group 6 | Group 7
Group Projects - Blood Cell Biology - Updated 21 April  
This year's main topic is Blood Cell Biology. Each group should discuss with group members the specific sub-topic that will be covered by their project.

Here is a list of some of the cell types (Structure and Function)

PuMed citations PuMed Central citations PuMed Central note
Note - that while full publications are available online at PuMed Central, not all these publications allow reuse. You should still always identify the copyright statement within the actual article that allows reuse. Many research labs that receive government grants are required to make their published research available on PMC, this does not mean that the publicly available copy content can be used in your projects.

Remember - No easily identifiable statement usually means that you cannot reuse.


Examples from Megakaryocyte references on PubMed Central

Embryology - content cannot be reused but a useful resource about cell development.

Histology - images these can be reused in your projects.

Group Assessment Criteria  

Group Assessment Criteria

  1. The key points relating to the topic that your group allocated are clearly described.
  2. The choice of content, headings and sub-headings, diagrams, tables, graphs show a good understanding of the topic area.
  3. Content is correctly cited and referenced.
  4. The wiki has an element of teaching at a peer level using the student's own innovative diagrams, tables or figures and/or using interesting examples or explanations.
  5. Evidence of significant research relating to basic and applied sciences that goes beyond the formal teaching activities.
  6. Relates the topic and content of the Wiki entry to learning aims of cell biology.
  7. Clearly reflects on editing/feedback from group peers and articulates how the Wiki could be improved (or not) based on peer comments/feedback. Demonstrates an ability to review own work when criticised in an open edited wiki format. Reflects on what was learned from the process of editing a peer's wiki.
  8. Evaluates own performance and that of group peers to give a rounded summary of this wiki process in terms of group effort and achievement.
  9. The content of the wiki should demonstrate to the reader that your group has researched adequately on this topic and covered the key areas necessary to inform your peers in their learning.
  10. Develops and edits the wiki entries in accordance with the above guidelines.

Group 3: User:Z5019595 | User:Z5019962 | User:Z5018925 | User:Z3461911

Discussion

Z3461911 (talk) 20:06, 22 March 2016 (AEDT): Hey guys, just wondering which subtopic we should do. If anyone of us also do immuno, the lymphocytes should be right up our alley. What do you guys think?

Z5019962 (talk) Hey guys! Looking forward to working with you all. I don't do immunology but I was actually thinking that lymphocytes would be an interesting topic, or my other thinking was erythrocytes, becauseI think there would be alot of information in that area. I'm not too fussed on the subtopic, so if anyone has strong preferences, we can go with that.

Z3461911 (talk) 08:50, 24 March 2016 (AEDT): well since no one else has seen this yet I guess we will have to settle with either lymphocytes or erythrocytes.

Z5018925 (talk) 11:21, 24 March 2016 (AEDT) http://www.nature.com/nri/journal/v15/n3/full/nri3801.html

Z5018925 (talk) 11:21, 24 March 2016 (AEDT) That's a link for history

Z5018925 (talk) 11:28, 24 March 2016 (AEDT)Looks useful http://www.ncbi.nlm.nih.gov/books/NBK10757/?depth=10


Z5019962 (talk) Hey guys, this review article has some good background info in B cell structure, function and history - might help! http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2518873/

peer review

z3463953

A lot of good quality information but a very bland page. Here are some notes: - History is not very extensive - B-cell development and B cell subset image is very small! I would make it twice as large (800px). And maybe describe it in text more - Section: development, 3rd paragraph: spelling error - Instead of using in text referencing, you should use footnotes (easier for the reader to find the references). Remember it doesn’t have to be a pubmed affiliated article to be made a footnote, just put in “[2]” - Section: development. You introduce the term L chains with no description, the reader may have no idea what that is. Make sure you describe newly introduced terms! - There is an underwhelming amount of images used. Images should be used for: o B cell activation o Mind map of different B cells o Different antibodies - Tables are bland as well, try adding some colour! - Evidently you must finish the immunodeficiency/ and b cell cancer sections! - Also go into more depth about the biotechnology applications of B cells and don’t forget references!

Lab 3 Assessment

Jing z3461911

Role of B cells in the pathogenesis of systemic sclerosis[1]

In this article it is speculated that B cells play a significant role in the pathogenesis in systemic sclerosis. B cells are therefore observed in both within damaged organs and at a systemic level to determine their role in the inflammatory and fibrotic phases during systemic sclerosis. Through this observation, the B cells subset, marginal zone B cells, are found to be harmful through their synthesis of pro-inflammatory cytokines such as TGF beta and IL-4. These cytokines are also growth promoting cytokines which in turn lead to the development of systemic sclerosis.

B cell-targeted therapy with anti-CD20 monoclonal antibody in a mouse model of Graves’ hyperthyroidism[2]

Graves’ disease is characterised by an overproduction of thyroid hormones and thyroid enlargement, which is a result of B-cell- and T-cell-mediated inflammation. This particular study (Ueki et al., 2011) administered anti-mouse CD20 monoclonal antibodies in mouse models of Graves’ disease, which eliminated B cells from the periphery and spleen. In effect, this suppressed serum immunoglobulin levels, splenocyte secretion IFN-γ, and development of hyperthyroidism. B cell depletion was found to be highly effective in preventing disease development.

PAX5 promotes pre-B cell proliferation by regulating the expression of pre-B cell receptor and its downstream signaling[3]

This article examines the Pax5 gene and its role in the development in B cells. It is well known that Pax5 contributes to B cell development but the impact of Pax5 on pre-B cells is unknown. To identify this relationship, the Pax5gene was knocked out of mice and the levels of marker proteins present at various stages of B cell development were monitored. Most marker proteins were observed to be lower than if the Pax5 gene was still present. Due to the lowered amounts, a signalling cascade could not form and therefore the B cells were not able to develop from the pre-B cells.

Abnormal B-cell cytokine responses a trigger of T-cell-mediated disease in MS[4]

The depletion of B cells can have immune consequences are hypothesised to have influence on multiple sclerosis. This article explores this hypothesis by comparing B cell effector-cytokine responses in mulitsclerosis patients. These experiments were conducted both in vivo and ex vivo. Results showed low amounts of proinflammatory responses for cytotoxic and helper T cells. The remaining B cells then made up for these low amounts of T cells. From these results, the article states that lowered B cells mediate " bystander activation" of T cells which result in the relapse of multiple sclerosis.

z5021149

NF-kB inhibitor blocks B cell development at two checkpoints[5]

During development, B cells start in bone marrow and then move through different stages until they finally mature in the spleen. Various checkpoints, transcription factors and regulatory factors are utilized during this process to ensure only healthy b cells continue down the path of development. NF-kB is an example of a protein complex transcription factor that plays a role in b cell development. In order to identify when NF-kB was acting during development, Feng et al introduced an NF-kB inhibitor (IkBα) via a viral vector. What they found was that in subjects that received the viral IkBα, the reconstitution levels of b cells was much less in bone marrow and spleen compared to the subjects who did not receive the inhibitor. This lead to the conclusion that NF-kB plays a role in the development od B cells in the bone marrow, as well as maturation and survival in the spleen

The immunosenescence-related gene Zizimin2 is associated with early bone marrow B cell development and marginal zone B cell formation[6]

The Zizimin2 gene has previously been identified to be related to immuno-senescence and filopodia formation in immune tissues. Expression of the gene has been observed in aging mice. There has been little research into how the Zizimin2 gene actually effects the immune response and how the decline in expression of the gene leads to immuno-senescence. Matsuda et al generated Ziz2 knock out (KO) mice to examine what effects removing this gene would have on the immune response. when thy compared the KO mice to wild type, they found that the KO mice had a higher percentage of early bone marrow B cells, but a reduced number of mature marginal zone B cells. The Ziz2 gene clearly has en effect on marginal zone B cell maturation, but had little effect on the folical B cells. Marginal zone B cells play a role in fighting infectious disease by reducing the time that it takes the body to mount a response against the infectious substance. A decrease in the expression of Ziz2 with age may effect the hosts ability to fight off infectious disease by decreasing the fraction of marginal zone B cells.

Effects of lasofoxifene and bazedoxifene on B cell development and function.[7]

Initially, estrogen was seen as an effective treatment for menopausal women with osteoporosis. Estrogen does increase the bone mineral density in women with osteoporosis, however estrogen treatment has been linked with increased risk of endometrial and breast cancer. SERMs are a class of estrogen receptor agonist/antagonists, which act differently depending on the tissue type. Second generation SERMs such as raloxifene have been observed to increase BMD but not increase the weight of the uterus in mice. Estrogen has effects not only on BMD and uterine weight, but also on the immune system. Bernardi et al set out to investigate what effects third generation SERMs such as lasofoxifene (las) and bazedoxifene (bza) have on the immune system compared to traditional estrogen treatments. It was observed that while estrogen treatment lead to a decrease in B cell numbers across all of the developmental stages, while las and bza only effected b cells in the late stages of bone marrow b cell development and splenic transitional 1 b cells.Estrogen treated subjects also had an increase in antibody producing cells while those treated with las or bza did not.

Zinc transporter SLC39A10/ZIP10 facilitates antiapoptotic signaling during early B-cell development[8]

As B cells move through the different stages of development, various requirements must be met in order to for the cell to move down the path of differentiation. Zinc has long been know to be related to immune function as people with Zinc deficiency present with low immune function. While the link has been clearly established, the mechanism behind the lack in immune function has not been demonstrated. Miyai et all set out to find a mechanism behind zinc deficiency by examining the role of the ZIP10 zinc transporter. By down regulating the ZIP10 transporter, decreased levels of Zn were seen in the cell. This activated caspase activity and lead to the cell undergoing apotosis. Overall, the down regulation of ZIP10 lead to a decrease in the population of B cells. This ZIP10-mediated Zn homeostasis is vital for the survival of early B cells which go on to become functional immune cells.

z5019962

Article 1

Bruno, Tullia et al. "Antigen Presentation By Tumor Infiltrating B Cells Influences CD4 T Cell Phenotype And Function In Primary Lung Cancer Patient Tumors". Journal for ImmunoTherapy of Cancer 3.Suppl 2 (2015): P397.

This study looks at the role of B cells in non- small cell tumours, and how the correlation of improved survival with increased B cell levels provides some understanding of the function of B cells. It was shown that B cells within the tumour (TIL- Bs) present tumour autologous antigens, and polarized other cells to produce anti- tumour cells, such as T- helper cells.

Article 2

Shimabukuro-Vornhagen, Alexander et al. "The Immunosuppressive Factors IL-10, TGF-Β, And VEGF Do Not Affect The Antigen-Presenting Function Of CD40-Activated B Cells". J Exp Clin Cancer Res 31.1 (2012): 47.

B cells play an important role in immune stimulation, through their association with antigen- presentation. This article explores whether immunosuppression works against the immunotherapeutic role of B cells, or whether B cells retain their immunostimulatory function.

Article 3

Shimabukuro-Vornhagen, Alexander et al. "The Immunosuppressive Factors IL-10, TGF-Β, And VEGF Do Not Affect The Antigen-Presenting Function Of CD40-Activated B Cells". J Exp Clin Cancer Res 31.1 (2012): 47.

Teleost fish have a large mucosal surface, via which pathogens can enter the body. As a result of this, it is essential that these organisms possess a mucosal immune system that maintains the balance between pathogenic and non- pathogenic bacteria at these vulnerable points – B cell predominate in this defense system. This study looks at the important role of B cells in gut- immunity and the acquired immune response. It was found that B cells carry out their effect on the gut immune system through their capacity to differentiate into antibody secreting cells, producing immunoglobulins to target pathogens, and presenting antigens to T cells for destruction.

Article 4

Barsotti, Nathalia Silveira et al. "IL-10-Producing Regulatory B Cells Are Decreased In Patients With Common Variable Immunodeficiency". PLOS ONE 11.3 (2016): e0151761.

This article looks at the link between the absence of regulatory B cells and immunodeficiency, providing valuable insight into the importance of the function of these B cells in immunity. It was found that individuals with common variable immunodeficiency (CVID), generally presented with depressed levels of regulatory B cells, which results in reduced control of T cell activation and autoimmunity.

References

  1. <pubmed>2721390</pubmed>
  2. <pubmed>21235532</pubmed>
  3. <pubmed>27016671</pubmed>
  4. <pubmed>20437580</pubmed>
  5. <pubmed>15050028</pubmed>
  6. <pubmed>25729399</pubmed>
  7. <pubmed>26477271</pubmed>
  8. <pubmed>25074913</pubmed>