Monday, December 23, 2013
Sunday, December 22, 2013
|1. Macrophage Engulfing Apoptotic Cells|
Friday, December 20, 2013
|Malaria cases by country (6)|
|Life cycle of plasmodium falciparum (7)|
Thursday, December 19, 2013
Previous to the study by Beavis et al (2013), adenosine has been know to be produced from the breakdown of AMP by CD73 - a marker present on many types of cells. It has also been shown that anti-CD73 has resulted in delays in tumor expression, altogether rejection of tumor grafts in mice, inhibiting de novo carcinogensis, and preventing/reducing metastasis. In order to elucidate how exactly this immunosuppressive compound, adenosine, was suppressing tumor growth and metastasis, the authors set out to investigate adenosine in depth.
New Possible HIV Treatment reduces HIV-1 Infectivity with the use of GANP to mediate APOBEC3G Packaging in HIV-1 Virions
Wednesday, December 18, 2013
|Interaction of APOBEC3G/Vif|
|Figure 1. Population Distribution of Mutations|
After the treatment, she has not has any remission or signs of cancer but this is not the case for every individual in the study. It could be due to them having an immune response to the vector used but it is undetermined as to why it works for some and not others which is why a cure has not been announced. It is a promising treatment as many are researching and putting money into the effort to discover new properties. T-cell engineering does not cost as much as bone marrow transplantation so it does look like a promising avenue.
Autoimmune disease is associated with adaptive immune component dysfunction such as the B cells and T cells. The cells somehow pass through peripheral tolerance and cause a self reaction. Autoimmunity is determined by genetics, environmental, and hormonal effects that contribute to the disease. Many autoimmune diseases have been studied and examined but the biology behind them are not completely understood.
A major pathway is the CD40-CD40 ligand (CD154) because it is needed to activate many adaptive immune cells such as DC's, B cells, and T cells. This interaction has multiple functions and as costimulatory molecules, they are upregulated in several autoimmune diseases for example SLE (systemic lupus ertyhematosus). It was thought that disabling this interaction could be a new avenue of therapy for autoimmunity.
Caption: The basic polarization of T cells is shown in the following image with different cytokines determining the Th cell developed.
These iPSCs, once discovered, opened up those doors that ethical and moral questions shut for researchers. But, it was clear the iPSCs are different than hESCs and researchers had a fair bit of work in front of them to make sure that the iPSCs were at least comparable in the flexibility and thus utility of hESCs. This largely entailed experimenting with different environments and factors that the researchers would submit the cells to in order to create iPSCs. Eventually, researchers were able to derive iPSCs from more than just human skin cells (Yu et al, 2007), but other cells such as human urine cells (Zhou et al, 2012). As researchers have improved on these techniques, researchers like Morizane et al (2013) set out to investigate the quality of these iPSCs by injecting them into animals to investigate the utility of iPSCs as well as evaluate the benefits stem cells from one's own body may have on graft rejection or lack thereof.
In the study by Morizane et al (2013), the researchers used a primate model in order to evaluate the ability for autologous iPSCs and allogenic iPSCs to generate an immune response and engraft dopamine neurons in the primate midbrain. Like any other transplantation the immune system is an important player in the ability for the limb, cell, organ, etc. to engraft and become functional in the body. If recognized by certain immune cells in the body, the body can start attacking the transplant, reject it, and potentially damage the surrounding area in the process.
|Diagram of the HIV virus|
|Depiction of HIV spread from a DC to a T cell|
Saturday, December 14, 2013
Although it seems as if this disease's cause is well-known and can be modeled well in animals, effective therapies to MS have proven hard to develop - one reason for this is that MS is different in almost every patient as to when it is symptomatic or not. This variation is so great that MS is characterized into many types of the disease such as relapse-remitting MS (RRMS) which the patient experiences many symptoms for months and then relapses into a largely symptom free condition, only to repeat in the future. Further, secondary progressing MS (SPMS) is a type of the disease - when symptomatic - declines at a devastating rate. There are more types, such as some that do not relapse and a continual decline is observed. It has been hypothesized that the Epstein-Barr virus (EBV; commonly known to cause mononucleosis) has some influence on this stability of disease - although results have not been very conclusive. This variability in the disease, as you can assume, confounds scientists researching therapies and potential cures to this devastating disease.
In hopes of elucidating why this variability is so great in this disease and if EPV has a role in disease stability, Annunziata et al in Italy investigated the role of EPV-positive B cells in disease severity. By extracting B cells from patients with MS, they examined the spectrum of antibodies that were produced by the MS patients of varying disease type. Initially, they identified 7 monoclonal antibodies (mAbs) that were found to bind a specific epitope (105-120) in one of the components of myelin that surround the neurons, MBP (myelin-basic protein). They chose this epitope of MBP because these mAbs were detected in the more 'stable' MS patients - and hoped to find something unique in these patients' body responses to the disease. Further testing included myelin-reactive T cells from MS to be evaluated in environments of the mAbs. Interestingly enough, only 3 mAbs showed dose-dependent inhibitory effects to the T cells - which are thought to contribute to the damaging environment in MS.
Friday, December 13, 2013
Thursday, December 12, 2013
Tuesday, December 10, 2013
|"Types of Brain and Spinal Cord Tumors in Children." Johns Hopkins Medicine. |
Johns Hopkins University, Hospital, and Health System, 2013. Web. 10 Dec. 2013.
Allergic diseases develop when a person's immune system becomes sensitized to a normally harmless antigen. Type I hypersensitivity is a category of allergic reaction in which CD4+ Th2 cells that interact with these antigens stimulate B-cells to produce
Immunoglobulin E (IgE) antibodies. These antibodies will then mark the specific antigen for destruction by other immune cells.+ Once the individual has been initially exposed and developed the specific antibodies, a subsequent exposure to the allergen will result in an allergic reaction. For more information, click here.
|Mechanisms of Allergic Response|
Monday, December 9, 2013
Thursday, December 5, 2013
Wednesday, December 4, 2013
|Figure 1: HIV replication in a cell. It is able to dump its|
contents into the cell, reverse transcribe its RNA,
integrate it into host DNA, and use the host to create new viral copies.
|Figure 2: Timeline of HIV infection. As viral RNA increases,|
CD4+ cells decrease. A latent period exists where the
person may not know they are infected
until their cell count reaches a certain point.