Talk:2016 Group 6 Project

From CellBiology


General Organisation

Factsheet & Roadmap


Drive: (View Only link, edit link will be provided in private)

Basic questions needing answering

What is the shape of a T cell like? What do the T cells differentiate from? Where do they mature? Thymus Locations where they reside?


post resource link in the respective subsection (otherwise we'll get a real mess of resources) and include a short comment what it should be usesful for


Introduction links

PMID 26635800 - T Lymphocyte Migration: An Action Movie Starring the Actin and Associated Actors.

PMID 25523165 - Role of T lymphocytes in hypertension.

PMID 24556090 - Metabolism of activated T lymphocytes.

PMID 24672781 - A role for T-lymphocytes in human breast cancer and in canine mammary tumors.

PMID 24003925 - The targeting of β-cells by T lymphocytes in human type 1 diabetes: clinical perspectives.


History/ other T cell links

PMID 25746046 - Orchestration of invariant natural killer T cell development by E and Id proteins.

PMID 25396352 - Molecular regulation of effector and memory T cell differentiation.

PMID 25727290 - Innate memory T cells.

PMID 17972353 - A brief history of CD8 T cells

PMID 17972355 - Regulatory T cells – a brief history and perspective

PMID 15140026 - Events that led to the discovery of T-cell development and function--a personal recollection.

PMCID: PMC1857272 - Th1 and Th2 subsets

Common Structure and Function

Type of T-Cells

Cytotoxic T Cells

PMID 26161391 - Functional Alteration of Natural Killer Cells and Cytotoxic T Lymphocytes upon Asbestos Exposure and in Malignant Mesothelioma Patients

PMID 25973438 - Epigenetic control of interferon-gamma expression in CD8 T cells.

PMID 25834833 - The story of CD4+ CD28- T cells revisited: solved or still ongoing?




Clinical Implications and Disease

Helper T Cells




Clinical Implications and Disease

T Regulatory Cells




Clinical Implications and Disease

Natural Killer T-Cells




Clinical Implications and Disease

PMID 22294696 - Interleukin-22 is produced by invariant natural killer T lymphocytes during influenza A virus infection: potential role in protection against lung epithelial damages, Paget, C., et al.

PMID 22442383 - Microbial exposure during early life has persistent effects on natural killer T cell function, Olszak, T., et al.

PMID 12021841 - Regulation of autoimmune disease by natural killer T cells.

PMID 16412042 - The natural killer T lymphocyte: a player in the complex regulation of autoimmune diabetes in non-obese diabetic mice.

Current Research, Future Directions and Conclusion



Note: I haven't checked the copyright on any of these yet. Most are reviews and will need to be referenced accordingly

All T cell links

PMID 7006707 - Human T-lymphocyte growth factor: regulation of growth and function of T lymphocytes.

PMID 26913033 - Biophysical Aspects of T Lymphocyte Activation at the Immune Synapse.

PMID 24099302 - MicroRNA regulation of T-lymphocyte immunity: modulation of molecular networks responsible for T-cell activation, differentiation, and development.

PMID 8727107 - T-lymphocyte interactions with endothelium and extracellular matrix.

PMID 6389597 - Human T lymphocyte subsets. Functional heterogeneity and surface recognition structures.

Natural Killer T cell links



Z5018866 (talk) 22:48, 25 April 2016 (AEST)

  • Added in a table for history, I think it might be easier to read and understand just with a table, as the history is more of a minor section and will be good to break up text as much as possible?
  • Let me know if you have any key findings or points to add and I can find a reference for it and add it too.
  • I think nomenclature of t cell would be covered in intro or common section as they all develop in thymus.
  • I'll add in a graph of articles too

z5105710: As stated in the facebook group i propose a change of structure of the Tc subheadings, from 2. struc. 3. funct, as the first thing I want to now about a cell is its function, then how it looks like and then how it is generated, and not the other way arround

z5105710: Guys, just adapted the structure to what we discussed. Feedback welcome. Cheers!

Z5018866 (talk) 15:11, 13 April 2016 (AEST) Hi, just for the structure of the history section do you guys think this is a good outline to follow:

  • When they were discovered and through what experiment
  • Nomenclature?
  • Key studies following the discovery
  • Potential Breakthrough findings since - if I can get enough key dates put it into a table

Also a lot of other groups have included the trends in research of that area, like how many articles on their topic over the year, not sure how they did this (wouldn't be hard to figure out) but do you think this would be good to have too?

z5105710: Sure thing, looks good for me. Make a short timeline and include fun facts. Dont do too much future, we dont want redundancy, we have a seperate heading for future directions

Z3465531 (talk) 18:02, 24 March 2016 (AEDT) Hi everyone, I expected to have work on Good Friday, but it turns out that I do not and that I am available. If we need to meet at any time, I am available.

Z3465531 (talk) 15:41, 24 March 2016 (AEDT) Hi Everyone, I apologize again that I will not be able to meet tomorrow to discuss the outline. I am definitely available by phone or skype after 5 pm or perhaps for I could step away for 15 minutes during work if you shoot me a message. I have looked at the feedback for the other projects that were done in 2015, and I think we should be have an outline that looks something like the following:

z3329177 I'm in the main library till 6 i guess, if anyone can meet i would love to join.

Proposals for Structure


1. Banner

2. Introduction

3. History

4. Add common structure and function

5. Types

5.a. Structure

5.b. Mechanisms and development

5.c. Functions and roles in the body

5.d. Clinical implications and diseases

6. Current research, future directions and do as conclusion

7. Glossary

8. References

In terms of dividing work I think we should do a type of t-cell each, making a glossary and doing references as we go along for our sub type. For the common structure and function and current research we can collaborate at the end Someone can do the intro and someone can do history whilst others can do the smaller subtypes of t cells


1) Banner Heading (as in Group 1 2015)

2) Introduction (as in Group 1 2015, or with timeline graphic as in group 4 with internal referencing, or video as in group 5, careful with citing though) Be sure to cite textbook if used

3) History (Emphasizing research techniques)

4) Types of T Lymphocytes

5) Structure (as in Group 1 2015)

6) Function

7) Malfunction of T-lymphcyes – investigation of T-Lymphocyte malfunction as a causative agent of disease

8) Current Research – (Possibly switched in order with clinical significance, we’ll see how it feels, good example Group 5 2015 with collapsible tables) -

9) Clinical Significance (as in Group 3 2015)

10) Future Directions (Possibly unify this with the conclusion? Plenty of examples)

11) Conclusion (closing section)

12) Glossary (as in Group 1 2015)

13) References

What does everyone think?


1)Titel Picture

2) Introduction

4) History (short! keep it on the history of discovery of structure and function, as this is a cell biology class)

3) Common Characteristics (Structure and function of T-Cells compared to other BC's, not too much as specific structure and function of each T-Cell type will be covered in Subsection and they are very different from each other)

Surface Proteins TCR ...

4) Development (Short, not too much immunology)

5) Types (focus on structure and function, Activation, mechanism of action, involved pathways etc.)

6) Clinical Significance (focus on cell biology pathways in the development of the disease)

7) Current research (Involved research centers, current theories related to cell biology of T-Cells etc.) Elaborate this section, he put emphasis on it on a) the lecture b) criticism to former projects


I was looking at the structure, i will add a bit more,but the format could be roughly like this

1. General information (about t-cells, types etc.)

2. History (early and current researches, future expectations)

3. Cell structure

4. Function and mechanisms

5. Related diseases

6. Glossary

7. References

Division of Topics:

Helper - z3329177

Cytotoxic - z5018866

Memory - z3465531

Suppressor - z5105710

Natural killer

Mucosal associated invariant

Gamma delta T cells -

Suggestions for subtopic

z5105710: T Regulatory Cells: I

z3465531: T Regulatory Cells would be good. Red Blood Cell, Neutrophil, Eosinophil, Basophil, or Monocyte/Macrophage would be great because they always seem to be relevant to our studies. I'l be happy to go with whatever the group decides.

z5018866: I am more than happy to do T regulatory cells, as it would be great to do a topic that someone has a particular interest in. If there isn't enough on t reg cells alone we could maybe do T cells as a whole and z5105710 you could potentially focus on your interest of t reg cells.

z3329177: I'm happy with the topic, because there are many of articles about t-cells that we can access. For the T-Regulatory cells, i think that it is interesting topic, but i will need to learn more about it to be honest.


- Do not cite a review article has having findings. "As reviewed by" is more appropriate terminology. (As in This reference (Biochemistry of tropoelastin. Vrhovski B, Weiss AS. Eur J Biochem. 1998 Nov 15;258(1):1-18. Review. No abstract available. PMID 9851686 ) is a good review article to introduce your topic. One key point is that it is a "review" not original research and should have been cited as such. For example "as reviewed in" or "see review". It is important to discriminate between original research articles and reviews in your writing., group 3 of 2015)

- At all times, remember: How is this sentence related to our topic/subtopic and what are the consequences thereof. Bspw Group 3 2015 made subsection of Vit. A deficiency but didn't explain what this had to do with their exact topic

- At least 1 image on the page should be a student drawn image (e.g flow diagram, power point slide of the cell structure).

- Remember to give all uploaded content an appropriate name.

- Any time that you see nomenclature in an article that is not the current nomenclature (eg. MSDS instead of SDS), that means the article is old and should not be used.

- Avoid add unnecessary detail explaining biological processes that not directly related to the topic (e.g. the description of translation in Group 1 2015)

- It might be a good idea to add "additional information" collapsible boxes (as in Group 3 2015)

Lab 3 Assessment


1. Summary: Cathepsin B controls the persistence of memory CD8+ T lymphocytes, Byrne, S. M., et al. [1]

This study investigates the mechanisms by which memory T lymphocytes persist, even in the absence of antigen.

The findings indicate that one of the major limiting factors to memory CD8(+) T cell populations is the stability of the cell lysosomes. The genes IL-15 and IL-7 contribute to the production of serine protease inhibitor (Spi) 2A, which inhibits cytosolic cathepsin and thus inhibits apoptosis. In animal models, Spi2A inhibition results in less CD8+ T lymphocyte maturation and less homeostatic proliferation as well. The experimental results indicated that Spi2A is required in order for the memory CD8(+) T lymphocytes to maintain population numbers after viral infection and that one specific mechanism of action is protection from lysosomal breakdown via cathepsin B inhibition. Furthermore, it was found that T cells deficient in Spi2A could have their homeostatis restored by concurrently blocking cathepsin B, which strongly suggested that the physiological target of Spi2A was indeed cathepsin B.

The relevance of this topic to T lymphocytes, specifically memory T lymphocytes, is manifold. The primary function of memory T lymphocytes is to persist within the organism until such time as they are necessary to promote a fast, powerful targeted response to a second infection. If the population of the memory T lymphocytes is allowed to deplete, then immunological memory will not remain. If, on the other hand, memory T lymphocytes proliferated over abundantly, then this would be a likely mechanism for the development of possible leukemia.

2. Summary: The majority of HIV type 1 DNA in circulating CD4+ T lymphocytes is present in non-gut-homing resting memory CD4+ T cells, McBride, K., et al. [2]

This study investigates the locational distributions of integrated HIV-1 DNA copies within memory CD4+ T lymphocytes for the purposes of better understanding the efficacy of disease treatments.

A proposed site of prominent HIV-1 replication with Memory CD4+ T lymphocytes is the gut-associated lymphoid tissue, where such cells tend to recirculate. The researchers of this study hypothesized that regulatory T cells and activated CD4+ T lymphocytes tend to recirculate and disproportionately make up a source of the HIV-1 reservoir, serving as a difficulty needing to be solved in any possible eradication of the disease.

Real time polymerase chain reaction was used to localise HIV-1 DNA within the human immune cells. More than 80% of total HIV-1 DNA was found in non-gut-homing CD45RO+ memory T lymphocytes, while less than 10% was found in regulatory T cells and CD38+ activated memory cells. The researchers found that most of the HIV-1 DNA was present in non-gut homing resting CD(+) T cells. The findings of the experiment are significant because they work toward better understanding the locational pathogenesis of HIV-1 in memory CD4+ T lymphocytes, which is necessary for developing a cure.

3. Summary: Interleukin-22 is produced by invariant natural killer T lymphocytes during influenza A virus infection: potential role in protection against lung epithelial damages, Paget, C., et al. [3]

During viral infections, invariant natural killer T (iNKT) cells are a type of non-conventional T lymphocyte that plays a key role through quickly producing cytokines. While the mechanism of their action is not entirely well known, it has been proposed that they play a useful role during influenza A virus (IAV) infection.

The findings of the article support that iNKT cells produce IFN-γ and IL-22, cytokines critical to muscosal immunity. The specific mechanisms of the production and mediation of these cytokines are investigated, especially with respect to the morality of those infected by the virus. It was demonstrated in vitro and vivo, at least during early IAV infection, that IL-22 helps to prevent epithelial cell death in a IAV-infection of the airway. In total, iNKT cells were revealed to provide a quick source of IL-22 that possibly is critical to protecting the lung epithelium. These findings are significant to better understanding how T-lymphocytes, and specifically natural killer T lymphocytes, play a role in proactively protecting from early infections in critical exposed areas, such as the lungs.

4. Summary: Microbial exposure during early life has persistent effects on natural killer T cell function, Olszak, T., et al. [4]

This study investigated the importance of microbial exposure at a young age to the function of natural killer T cells, which are supposed to play a critical role in diseases relating to the immune system such inflammatory bowel disease (IBD) and asthma.

The findings of the article are that germ-free (GF) mice tended to accumulate invariant natural killer T (iNKT) cells in the lungs and in the lamina propria of colon, increasing morbidity as compared with specific pathogen-free mice. Also, the GF mice had increased intestinal and pulmonary expression of CXCL16, a chemokine ligand associated with increased iNKT cells of the mucosa.

On the other hand, when neonatal GF mice were colonized with conventional microbiota, the mice tended to be protected from iNKT accumulation within the mucosa and associated pathogenicity. The results of the experiments as a whole suggested that contact with commensal microbes by a critical early age are crucial to developing a healthy levels of mucosal iNKT. These findings are significant to better understanding iNKT cells because they address both the natural function of iNKT cells in providing resistance to environmental exposures, but the experimenters also investigate the double edged nature to this immunity. If a the host fails to interact with any conventional microbiota during the early stages of life, then the natural killer T-cells themselves seem to be a source of pathogenicity. The results of the experiment provide crucial insight for better understanding T lymphocytes as a whole.

Migratory challenges faced by T cells [5]


  1. <pubmed>22745374</pubmed>
  2. <pubmed>23971972</pubmed>
  3. <pubmed>22294696</pubmed>
  4. <pubmed>22442383</pubmed>
  5. <pubmed>26635800</pubmed>


1. Summary: Folate-mediated chitosan nanoparticles containing the IP-10 gene enhance melanoma-specific cytotoxic CD8+CD28+T Lymphocyte responses, He, J., “et. al.” [1]

In the study promising combination treatments for malignant melanomas are explored using adoptive immunotherapy with Cytotoxic T lymphocytes (CTL).

The study aimed to increase the CTL anti-tumor response by inducing melanoma TRP2-specific CD8+CD28+T cell in combination with folate-modified chitosan nanoparticles containing Interferon-y-inducible protein-10 (IP-10). IP-10 plays a role in chemotaxis particularly for CD8+ T cells towards the tumor [2][3]. The chitosan molecules where prepared with a IP-10 gene from a mouse and the TRP2-specific CD8+CD28+ T cells co-cultured with artificial antigen presenting cells, due to cost and efficiency. Affected mice were treated with one therapy, both or a saline control, with tumor size and survival times measured. Other immune cells were measured and TUNEL techniques used to determine proliferation and angiogenesis.

Overall the combination of the two therapies increased the anti-tumor response and hindered the advancement of the melanoma in vivo. Inhibiting growth and proliferation whilst promoting apoptosis of tumor cells leading to an extended survival time for the mice than either therapy alone. With the chitosan nanoparticles creating a chemotaxic by inducing IP-10 secretion, resulting in recruitment of CD8+ t cells in the tumor area angiogenesis and proliferation were reduced.

2. Summary: Delivery system of CpG oligodeoxynucleotides through eliciting and effective T cell immune response against melanoma in mice, Sun, W., “et. al.” [4]

Through the addition of a C-class CpG ODN-685 (oligodeoxynucleotides) the study aims to explore the effects on anti-tumor activity in melanoma inoculated mice as well as prophylactically in healthy mice to ultimately improve the immunogenicity of the whole tumor cell lysate developed as a vaccine for tumors, whilst. The CpG ODNs are involved in stimulating the early immune responses with T cell activation occurring during their transport to the immune system. There were two groups of study, prophylactic – which were given tumor cell lysate, CpG ODN, tumor cell lysate plus CpG ODN or PBS as control. At a later stage were given tumor cells. The other therapeutic group was inoculated with melanoma tumor cells and then received a treatment. Tumors were either inoculated in hind leg or peritoneum of mice. Subcutaneous and intraperitoneal melanoma affected mice did not respond to tumor lysate or CpG ODN but when combined an immune response was triggered. This led to longer survival time and prevented tumor spread to through the abdominal cavity. Upon analysis of splenocytes the lysate only group displayed anti-tumor effects whilst the CpG ODN alone did not however, when used in conjunction an enhanced response was displayed. Suggesting assistance from CpG ODN in stimulating a cytotoxic immune response. CD4+ / CD8+ T cells increased significantly after tumor inoculation signifying their involvement in immune response and when CpG ODNs where combine with tumor lysate a strong specific Cytotoxic T lymphocyte response was generated. It was concluded that CpG ODN-685 could be effective in increasing immunogenicity of tumor vaccines against melanoma.

3. Summary: Spinal cord T-cell infiltration in the rate spread nerve injury model: a time course study, Gattlen, C., “et. al.” [5]

Infiltration of the spinal cord by T-cells after SCI [5]

In this study Gattlen et. al. explored the immune response following a spared nerve injury (SNI) [6] in mice, in particular microglia, T-lymphocytes and cytotoxic T-lymphocytes responses. The study looks at the relation between different immune cell types and their role in pain and chronic pain. Levels of microglia (Iba1), T-lymphocyte (CD2) and cytotoxic T-lymphocyte (CD8) were measured through various techniques such as measuring gene expression and immunofluorescence.

Microglial reactivity gene expression was unregulated for a prolong period, whilst microglial proliferation measured through immunofluorescence was only increased sharply on day 2. Inflammatory genes were regulated following the SNI with pro-inflammatory factors such as interleukins being increased soon after injury and typical anti-inflammatory factors began to increase at a later stage. Following the SNI CD2 and CD8 cells were counted in the dorsal horn to detect T-cell infiltration into the spinal cord however, a significant difference was not found. This is comparable to a spinal cord injury where T-cell infiltration is displayed.

The increase of anti-inflammatory factors could be a factor in the resolution of the inflammation [7]. Increased excitability in the lamina neurons of the spinal cord has been linked to the increased presence of Pro-inflammatory factors [8]. From this the study concluded that further study should focus on the transition from pro- to anti- inflammatory phases of the microglial cells.

4. Summary: Eliciting cytotoxic T lymphocytes against human laryngeal cancer-derived antigens” evaluation of dendritic cells pulsed with a heat-treated tumour lysate and other antigen loading strategies for dendritic cell based vaccination, Wei, F., “et. al.” [9]

With the goal of improving the antitumor immunity though optimizing antigen loading of current dendritic cell (DC) vaccinations, Wei et. al. explore the value of various dendritic cell vaccinations comprised of whole tumor cells or their derivatives. Through antigen loading DCs tumor-associated antigen (TAA) specific t-cells and cytokine production can be induced. DCs pulsed with tumor cell supernatant (DC-TCS), whole-cell tumor stressed lysate (DC-TSL) and irradiated tumor cells (DC-ITC) where the three different types. It was found that DC-TSL induced strongest responses for TAA-specific T-cells, Th1 cytokine production, and cytotoxic T lymphocyte activity. Making it the most efficient of the three tested for laryngeal squamous cell carcinoma. DC-TCS and ITC inhibited T cell activation however, had limited capacity for CTL activity.

DCs have a potent antigen presenting capacity, which are taken advantage of in the vaccines that have shown promising clinical results [10]. However, a percentage of patients remain insensitive to the therapy, where further research can develop the immunogenicity of these current vaccinations.


  1. <pubmed>27022421</pubmed>
  2. <pubmed>18723067</pubmed>
  3. <pubmed>21802343</pubmed>
  4. <pubmed>26918036</pubmed>
  5. 5.0 5.1 <pubmed>27005622 </pubmed> Cite error: Invalid <ref> tag; name "PMID27005622" defined multiple times with different content
  6. <pubmed>19923276</pubmed>
  7. <pubmed>10767254</pubmed>
  8. <pubmed>18480275 </pubmed>
  9. <pubmed>26795730</pubmed>
  10. <pubmed>12633662</pubmed>


1. Summary: Defining characteristics of classical Hodgkin lymphoma microenvironment T-helper cells, Greaves P, et. al. [1]

This article shows that how the t helper cells acts in the diseases such as hodgkin lymohoma. The hypothesis that TH-infliltrate is expressing TH1 marker-rich rather than TH2-enriched in hodgkin lymohoma miroenvironment. The method that they used was gathering the samples from the CHL and RLN patients. The sample cultured based on technique developed for proliferation tumor infiltrating lymphocytes. The way of examine is looking at amount of the TH1 and TH2 associated with CCRs. The result of the experiment was that TH1 associated CCRs more than TH2 association with CCRs. This result proves that hypothesis that CHL express more to TH1 active and suppressed TH2 action. This study could give potential diagnostic, prognostic and therapy on CHL.

2. Summary: Brain Glycolipids Suppress T Helper Cells and Inhibit Autoimmune Demyelination, Mycko MP, et. al.[2]

Sulfatide treatment suppresses EAE. A, B, CD1d-deficient mice sensitized for EAE with MOG35–55 were treated with five intravenous injections of sulfatides or vehicle[2]

The summary of this article is that autoimmune demyelination disease such as multiple sclerosis. Myelin in the CNS contains proteins and lipids. These component could recognise as foreign by immune system. Autoimmune demyelination is the term that our immune system attacks our myelin. This research found inhibition of sulfatides dependent navie T helper cells. The sulfatides are consisting major component of myelin glycolipids. The effect of sulfatides was not related to necrosis or apoptosis but they are upregulating two transcription factors in early growth of T cell. This research found that Sulfatides inhibit navie T cell. Moreover, glycolipid 3-sulfate group was essential for the T cell suppression, and the T cell inhibition was galectin-4-dependent. The Th17 that is known as major effect for autoimmune demyelination is inhibited by sulfatides. Therefore, following result shows that sulfatides can prevent autoimmune demyelination. It could be relevant for future treatment of the MS.

3. Summary: Follicular T helper cells and humoral reactivity in kidney transplant patients, de Graav GN, et. al. [3]

This article demonstrate that Tfh cells may mediate humoral alloreactivity, and it also presents in immunosuppressed environment. This research wants to find the humoral alloreactivity of Tfh cells regulation in kidney transplant patients, unlikely current research found that B cell is main role in alloreactivity in kidney transplantation. Tfh cells gives differentiation of B cells by IL-21. They observe the numbers and function of peripheral Tfh cells in patients before and after transplantation. The research using the relationship with the presence of DSA and Tfh cells. The result shows that the remaining number of Tfh is stable after transplantation. However, their IL-21 producing capacity is decreasing under the immunosuppressive drugs, and also during the biopsies the Tfh cells co-localized with B cells and immunoglobulins in follicular-like structures.

4. Summary: Microbe driven T-helper cell differentiation: lessons from Candida albicans and Staphylococcus aureus, Zielinski CE. [4]

The Th1 and Th2 cells are discovered about 3 decades ago, but now we know that more of Th cells present, such as Th17 which is very important role in IL-17 induced recruitment of neutrophils, and also it is involving in destroying bacteria and fungi. However, this Th17 cells are also involving in pathogenesis of autoimmune disease. The differentiation of human Th17 cells are depending on the microbial antigen such as C. albicans and S. aureus. The C. albicans specific Th17 cells are dependent to IL-1β, but not in S. aureus specific th17 cells. The C. albicans induces pro-inflammatory Th17 cells, and this is incapable of self-regulatoryIL-10 production, unlikely S.aureus induces anti-inflammatory Th17 cells, and also produce IL-10. Having knowledge that how the microbes induces t-cell will be very important to therapeutic method for immunomodulation strategies.


  1. <pubmed>24004665</pubmed>
  2. 2.0 2.1 <pubmed>24948818</pubmed>
  3. <pubmed>25557528</pubmed>
  4. <pubmed>25040443</pubmed>


1. T lymphocytes need less than 3 min to discriminate between peptide MHCs with similar TCR-binding parameters, Brodovitch, A., et al. [1]


Brodovitch et al. investigated the kinetics of the interaction between MHCs and TCRs. MHC and TCR interaction plays a crucial role in the foundation of "immunological synapses" and discrimination of self and non-self. 1G4 TCR carrying human T-Lymphocytes are dropped on a surface functionalized with various different types, formes (diamonds, squares, crosses) and amounts of pMHCs. To determine the time necessary to differentiate between the distinguished pMHC types, interference reflection microscopy (IRM) was used to quantify the spreading area in real time. The results indicate, that the differentiation process is completed already after 2 minutes, a reflection of how fast our immune system is able to process attacks on our system.

2. The direction of migration of T-lymphocytes under flow depends upon which adhesion receptors are engaged, Dominiquez, GA., et al. [2]


The movement of leukocytes within vascular environments has given invaluable insight in the progression of auto-immune diseases such as multiple sklerose. The effort of basic research has been promptly rewarded by the discovery of one of the most effective treatments against MS, a monoclonal antibody called Natalizumab, which opts against the delocalisation of lymphocytes from the blood stream into nervous tissue[3]. In the light of such discoveries, further emphasis has been placed on the research of Lymphocyte movement. This paper tried to observe the interaction between lymphocyte function-associated antigen-1 (LFA-1; αLβ2), very late antigen-4 (VLA-4; α4β1) and their ligands, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), cell adhesion molecules expressed on the vascular endothelial lining. VCAM and ICAM was printed on a silicone polymer (PDSM) to inquire, whether ligand type and engagement strenght would influence the migration direction. It was found that direction and cell polarity are well influenced by ligand type and engagement strenght.

3. Broad T-cell receptor repertoire in T-lymphocytes derived from human induced pluripotent stem cells, Chang, CW., et al.[4]


Induced pluripotent stem cells (iPSC) are one of the biggest promises nowadays. The standard approach, also used in this paper, is viral transfection with Oct3/4, Sox2, c-Myc, and Klf4 [5]. These are the four transcription factors with the power to push cells back to the initial steps of their development. The therapeutic options for iPS are mind-boggling, from Leukemia to Multiple Sclerosis, an uncountable number of diseases is a direct consequence of a malfunctioning immune system. Chang et al. achieved for the first time to induce pluripotent human T-Lymphocytes with expression of various different T Cell Receptors (TCRs). The number of TCRs decreases with the advancing T-Cell development, an increase of incorporation of different TCRs thus signals dedifferentiation. The observed iPSC showed normal patterns of differentiation, as shown in subsequent expression of CD7 and CD3. Furthermore, cytokine signaling strongly resembled natural patterns. The importance of the findings in this paper are emphasized if one takes into account one of the major difficulties with iPSC: directed differentiation. Current approaches focus on mimicking the natural cell environment and copy it from in-vivo to in-vitro, an approach which has been successfully applied by the authors of this paper.

4. Restrictions to HIV-1 replication in resting CD4+ T lymphocytes, Pan, X., et al.[6], a review


Schematic model of HIV-1 replication and restrictions thereof in activated and resting CD4+ T lymphocytes[6]

Inarguably one of the most important Type of T-Cells are Cells expressing a CD4 surface glycoprotein (not in the Paper, but on a side note: In the range of T-Lymphocytes, CD4 is mainly expressed by T-Helper cells, but also found on other Leukocytes, such as NK-Cells[7]). As reviewed in the paper, besides physiological functions, T-Helper Cells also serve as the main host for HIV1, but only as long as they are in a active state. Active T-Helper Cells primarily reside in lympnodes and replicate not only its own, but also the viral genome. As CD4+ T-Lymphocytes become inactive, a actin structure forms around the cell nucleus and the cell becomes insusceptible for HIV invasion. The review states the cell restriction factor SAMHD1, a deoxynucleoside triphosphate triphosphohydrolase, a key player in inactive CD4+ Cell defense against reverse transcriptase and insertion of viral genom into nuclear DNA.


  1. <pubmed>25782169</pubmed>
  2. <pubmed>25674729</pubmed>
  3. <pubmed>16510744</pubmed>
  4. <pubmed>PMC4020825</pubmed>
  5. <pubmed>16904174</pubmed>
  6. 6.0 6.1 <pubmed>PMC3698640</pubmed>
  7. <pubmed>16951326</pubmed>

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 6: User:Z5018866 | User:Z3329177 | User:Z3465531 | User:Z5105710