BioLegend Web Updates
Blog - The Chan Zuckerberg Biohub: Seeking to Cure All Diseases

Chan (left) and Mark (right) Zuckerberg. Image from Reuters/Stephen Lam.
©Thomson Reuters 2016.
 
A few months ago, we discussed Sean Parker and his Parker Institute for Cancer Immunotherapy. BioLegend is a key reagent contributor for this $250 million grant aimed at defeating cancer. Now in the new year, another key Facebook contributor is making headlines in research. If you’re not familiar with Mark Zuckerberg, his claim to fame comes from the creation of Facebook, a near ubiquitous app valued at an estimated $350 billion with 1.86 billion subscribers1. He and his wife, Dr. Priscilla Chan, have engaged in numerous philanthropic pursuits and made sizeable donations to this point, including2:
  • $1.6 billion to the Silicon Valley Community Foundation
  • $120 million to San Francisco Bay Area schools
  • $100 million to the Newark New Jersey school system
  • $75 million to the San Francisco General Hospital (where Priscilla worked)
  • $25 million to the Center for Disease Control
  • $20 million to the Education Super Highway
Now, Chan and Zuckerberg are seeking an incredibly lofty goal: to “cure, manage, or prevent all diseases” by the year 2100. This plan was started with the Chan Zuckerberg Initiative (CZI), a limited liability company that will be funded by 99% of the couple’s Facebook shares (an estimated value of $45 billion). This was announced in a letter to their newborn daughter in late 2015.
Read the full letter here.

He looks like a natural.
Image from Stanford Medicine.
With the CZ Initiative set up and funding plans in place, the couple announced the creation of the Chan Zuckerberg Biohub. The CZ Biohub (CZB) provides $50 million in funding for researchers based in the San Francisco area at UC Berkeley, Stanford University, and the University of California at San Francisco (UCSF). 750 researchers applied for the grants, but ultimately, 47 (who are listed here) are going to receive cash grants of up to $1.5 million3. Overall, the CZB is expected to receive $600 million over the course of ten years. The CZB also had some interesting provisions and choices for their grants. For example, some individual investigator awards were reserved specifically for non-tenured scientists, making it easier for newer scientists to obtain a grant without competing with more senior researchers. For those averse to either the teaching or grant writing process, the Biohub created lab-leader positions that are devoid of these responsibilities.
There are two main components to the CZB: the Infectious Disease Initiative and the Cell Atlas. The Cell Atlas’ goal is to document and characterize every single cell within every tissue and organ of the human body. One of the purposes of this is to understand the nature of a healthy cell, then analyze how certain diseases affect them. Once the atlas is completed, the CZB plans to make this information readily available internationally to all scientists. They cite new technological advancements in sequencing and CRISPR as reasons why the atlas can be completed now. With an understanding of the cell types, CRISPR may then allow them to specifically edit combinations of genes or study protein functions to observe their roles in disease4.
The CZB wants to create an expanded version of our Cell Markers page.
In recent years, the world has been caught off guard by sudden outbreaks like Ebola and SARS. Public outcry quickly followed as the demand for vaccines and answers rose. The Infectious Disease Initiative (IDI) looks to take action on this front by developing new drugs and using computer models to help design vaccines and analyze data. In addition, the IDI is looking to create a universal diagnostic test to help diagnose virtually any infectious disease.
The basis for this last objective stems from a patient case in 2014, where a 14 year old boy was infected with a bacterial encephalitis that attacked the brain. His illness came on precipitously as he was hospitalized for six weeks and then put into a medically induced coma. Thankfully, Dr. Charles Chiu and Joseph DeRisi, PhD, led a team to use next-generation sequencing to diagnose the patient’s cerebrospinal fluid and blood within 48 hours. They then compared the obtained sequences to patient samples in GenBank, discovering 475 distinct DNA sequences from the cerebrospinal fluid that belonged to the bacteria, Leptospira (for comparison, 3 million sequences were found to be human). Penicillin was administered and eliminated the infection. This was done without actual confirmation of the diagnosis as a standard clinical test wasn’t available at the time. It wasn’t until 5 months later that the CDC confirmed the doctors were correct on their Leptospira hypothesis5. The rapid advancements in sequencing affordability and speed are reasons that the IDI are bullish on the future of disease assessment.
The first phase of Leptospira infection and its symptoms may subside quickly, but the secondary phase can cause meningitis and encephalitis.
The Chan Zuckerberg Biohub is pushing boundaries with the new technology at hand, and it’s encouraging to see some of the leaders in technology (Zuckerberg, Parker, and Bill Gates to name a few) take such interest in fostering strong research environments. Do you have any additional thoughts on the Biohub? Is the goal of curing all diseases by 2100 possible? Let us know at tech@biolegend.com.
Contributed by Ken Lau, PhD.

References
  1. Why Facebook could one day be worth $1 trillion
  2. What you should know about Mark Zuckerberg’s Big Gift News
  3. Mark Zuckerberg’s Research Hub Just Gave 47 Scientists $50 Million to Fight Diseases
  4. Chan Zuckerberg BioHub Homepage
  5. UCSF Genome Experts Show Value of “Next-Generation Sequencing” in Diagnosing Infection
Click for Reuters Restrictions.


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New Web Page: Immuno-Oncology Research Tools
BioLegend provides an extensive array of research tools for immuno-oncology research. From Flow Cytometry Antibodies to Recombinant proteins, BioLegend’s reagents can be used to study many aspects of immune involvement in cancers.

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Podcast Episode - Cannibalistic Hamsters, Newly Named Species, and More Animal News!
This latest podcast covers interesting animal-related news, including cannibalistic hamsters and the nerdy names scientists have given to newly discovered species.

Topics

Corn turns wild hamsters into cannibals
Bathing chicken eggs in light makes for calmer chickens
Fistulated Cows
Malaria molecule makes blood alluring to mosquitos
New amoeba named after Gandalf
New crab named after Severus Snape and other nerdy animal names

Keywords: animals, corn, niacin, hamsters, chickens, malaria, mosquitos, HMBPP, Gandalf, amoeba, Severus Snape, pellagra, biolegend


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Video - Thinking Outside the Brain: Interactions Beyond the CNS
Description: Development proceeds in a tightly controlled manner regulated by diverse, but intersecting signaling pathways. A growing area of research examines the role of communication between the brain and surrounding systems to regulate development and function. This video, provided by The Scientist and cosponsored by BioLegend, brings together a panel of experts to discuss the role of these synergistic interactions. Topics covered include signaling between the neural and vascular systems during development, as well as the role of cerebrospinal fluid in regulating neurogenesis.

Keywords: CNS, CSF, Stem cell, neural progenitor cell, glia, cellular markers, nestin, beta catenin, tubulin β3



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New Web Page: Parkinson's Disease
Parkinson's disease is one of the most well-known neurodegenerative disorders among the 600+ disorders afflicting the nervous system. This page details the known associated proteins that contribute to the disease. BioLegend provides an array of world-class antibodies, ELISA kits, and recombinant proteins for Parkinson’s research.

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Blog - From Bugs to Bedside – The Rise of Cisplatin as an Anti-Cancer Agent
Peculiar observations initially made in Eschericha coli (E. coli, left) led to the development of cisplatin (right).
Image Credit: HealthyHearing.org
In our previous blog post, we featured the side effects related to an up-and-coming method to treat cancer – immunotherapy. The notion that the body’s immune system combats circulating tumor cells has been known for decades, and blocking barriers that dampen the immune system makes rational sense as a mode of therapy. The rise of immunotherapy to treat cancer culminated from decades of targeted research, with advancements in the fields of immunology and cancer research that were funded and designed to understand the etiology of the disease. With a large proportion of research funding allocated specifically for the goal of understanding and defeating cancer (research budget of the National Cancer Institute [NCI] for 2015 was just north of 5 billion, and expected to grow to over 6 billion by 20201), this infusion of resources will hopefully bring promising therapies that revolutionize cancer therapy in the future.
But did you know that a large majority of effective clinical agents that are currently being used in the clinic originated, not from these types of targeted research, but from those that had nothing to do with diseases? In some cases, completely by accident?

A prime example of this is the story behind cisplatin.


House. Fox Television.
It began in the 1960s in the Michigan State University lab of Dr. Barnett Rosenberg, who studied the effects of electric currents on bacterial cell division. One day, he decided to utilize platinum as the material of choice to hook up to the cathode/anode in an electric chamber containing a tub of E. coli, thinking that platinum will most likely not have any biological effects on its own on the bacteria. However, once he began running electric current through the chamber, he noticed something very peculiar happening to the bacteria – they had stopped dividing, and became elongated up to as much as 300 times their original length. Once they stopped running the electric current, the bacteria once again started dividing in the medium.

Dr. Barnett Rosenberg (1926-2009).
Image Credit: MSUToday
Dr. Rosenberg and colleagues initially believed that they had found a way in which they could manage bacterial cell division by controlling electric current. However, upon further investigation, they realized that it wasn’t necessarily the electricity applied to the chamber, but rather something specific about the platinum electrodes they used, and the compound being solubilized from the poles into the buffer. Dr. Rosenberg and colleagues published this intriguing finding in Nature in 19652, and eventually isolated the causative agent to be cis-[Pt(NH3)2(Cl)2] (originally identified as Peyrone’s Salt, named after Italian chemist Michele Peyrone who initially formulated the compound in 1845). Now this compound is referred to as cisplatin.
Applying this newly-found discovery of cisplatin’s ability to stop bacterial cell division, Dr. Rosenberg and colleagues tested cisplatin on rat sarcoma models, in which they identified its anti-tumor properties3. Remarkably, despite the compound being composed of a heavy metal, cisplatin was relatively well-tolerated in vivo. Meanwhile, transplatin (trans-[Pt(NH3)2(Cl)2], the stereoisomer of cisplatin, was acutely toxic and did not have anti-tumor effects.
Cisplatin (left) and transplatin (right). Cisplatin has anti-tumor effects, and transplatin is simply just toxic to the body.
Clinical trials for cisplatin began in 1972, and by 1978, it was approved by the FDA for use to treat testicular and bladder cancer. The clinical benefit of cisplatin, especially in testicular cancer, was astounding – it can cure up to 90% of cancers when detected early. Since 1975, the mortality rate of testicular cancer patients had declined by two-thirds, and this has largely been attributed to the introduction of cisplatin into the clinic4. Given the success of cisplatin, new platinum-based analogs of the compound including carboplatin, satraplatin, and oxaliplatin have since been developed and put into therapeutic use. They have been shown to have added benefits to cisplatin’s anti-tumor activity, including efficacy in multiple tumor types, with lowered toxicity. More recent research identified cisplatin’s mechanism of action, which acts by binding to DNA to generate intra-strand crosslinks. This results in alterations of the DNA structure which, upon undergoing replication, can generate DNA damage that ultimately elicit cell death in rapidly dividing cells. The mechanism also explains why transplatin didn’t have any anti-tumor effects – the chemical structure of the trans-form doesn’t bind to the DNA grooves like the cis-isomer.
From what began as an experiment that you might perform in a high school chemistry class came one of the most groundbreaking cancer therapeutic discoveries that has saved millions of lives (and counting). The rise of cisplatin in the clinic also exemplifies how scientific experiments that are seemingly unrelated to diseases can create an impact, not only in the clinic, but in future avenues for targeted research. Different forms of DNA damaging agents are widely used (with more being considered and investigated) in the clinic today. So who knows? Don’t be surprised if the next breakthrough therapy comes out of somewhere that is totally unexpected!

The next big cancer treatment coming out of nowhere?
Do you do research related to cisplatin and platinum-based analogs? DNA damaging agents? Let us know at tech@biolegend.com!
References
  1. NCI Budget and Appropriations
  2. Inhibition of Cell Division in Escherichia coli by Electrolysis Products from a Platinum Electrode
  3. Platinum Compounds: a New Class of Potent Antitumour Agents
  4. The "Accidental" Cure—Platinum-based Treatment for Cancer: The Discovery of Cisplatin
  5. Biography of Professor Barnett Rosenberg: A Tribute to His Life and His Achievements
Contributed by Kenta Yamamoto, PhD.


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New Web Page: Cell Health and Proliferation
Cell labeling probes (both antibodies and non-antibodies) can be used in a number of applications, including cell cycle, apoptosis, viability, cell proliferation, cell movement. Check out our upgraded Cell Health and Proliferation webpage to learn more about how these reagents work and how they can aid you.

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Podcast Episode - Rat Tickling, Peanut Allergies, and the Mesentery
The Talkin' Immunology podcast makes its return for the new year! We discuss peanut allergies, the new Mesentery organ, and the joy of tickling rats!

Topics

Introducing peanuts to children at young age may prevent allergies later in life
Meet your new organ: the Mesentery
Keeping the science honest on TV shows
Lying may wire your brain to keep lying
Rats enjoy a good tickle
Teen worms are like human teens
Transmissible cancer and genetic variations in Tasmanian Devils

Keywords: peanuts, food allergies, podcast, BioLegend, immunology, oral tolerance, hygiene hypothesis, mesentery, lying, tickling, Tasmanian devil, cancer



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Blog - Out of the frying pan into the fire? Immune checkpoint inhibitors can induce autoimmunity.
Perhaps you have heard of new immune-checkpoint therapies that harness the immune system to fight cancers such as melanoma, Hodgkin’s lymphoma and cancers of the lung, kidney and bladder. Rather than target the cancer cells directly, as chemotherapy does, these immunotherapies seek to co-opt the patient’s own immune system to fight the disease. These drugs take advantage of proteins (known as immune checkpoints) on some cell surfaces that allow them to escape immune surveillance. These checkpoints can shut down activated T cells and suppress the immune response. It turns out that some cancer cells express these same proteins – one of which is called PD-L1. When PD-L1 is expressed, cancer cells are ignored by the immune system and grow undisturbed1. In order to propel the immune system into action, patients can be treated with monoclonal antibodies against PD-L1, so-called immune checkpoint inhibitors, which lift the immune blockade against the cancer cell. T cells can then “see” the cancer cells and attack them. These therapies were hailed as the “Breakthrough of the Year” by Science magazine in 2013, and have produced startling results in many patients. For example, one patient who was diagnosed with non-small-cell lung cancer was treated simultaneously with two checkpoint inhibitors, and saw that his lung tumor shrunk by a third in only 4 months, and completely disappeared after 10 months of treatment2.
While information about these miraculous drugs has spread throughout popular news, what you may not have heard about is the collateral damage caused by these miraculous treatments. By relieving the blockade that prevents T cells from attacking cancer cells, T cells are also free to attack other body cells. These uninhibited immune systems have been shown to attack healthy organs such as the bowel, liver, lungs, kidneys, adrenal and pituitary glands and, in rare cases, the heart. Research is now showing that severe reactions occur almost 20% of the time in patients receiving treatment with a monoclonal antibody against another checkpoint marker, CTLA-43. Additionally, 30% of patients receiving anti-PD-1 treatment exhibit immune-related adverse events (irAE’s)4. When these drugs are used in combination, the incidence of irAE’s is even higher–more than 50%5!
Interestingly, one side effect has been the appearance of what one doctor thinks is a new form of Type I diabetes. Typically, the onset of Type I diabetes occurs between 6 and 12 years of age, leading it to be commonly called juvenile diabetes. Type I diabetes occurs as the immune system gradually but entirely destroys the insulin-producing beta cells of the pancreas. Patients treated with checkpoint inhibitors, however, are losing insulin production all at once. Moreover, these patients are often over 50, and are even as old as 83, defying the traditional age of onset of diabetes. Despite the age and rapidity of disease onset, these patients present with symptoms consistent with autoimmune diabetes, such as GAD65 and insulin autoantibodies6. This data indicates that the without the control of immune checkpoints, the body can turn on itself.

You’re saying I had cancer? And now I have diabetes? Bill Murray in Caddyshack sums it up.
Though reversible or maintainable with corticosteroids when identified early, these irAE’s can arise rapidly, be unpredictable, and confound ER doctors who are unfamiliar with the possible side effects of immunotherapy drugs. One patient receiving immunotherapy in L.A., for example, died in the ER after cold and flu-like symptoms exploded into an inflammatory response that her doctor called, “a mass riot” of her immune system2. Part of the reason why physicians are under-prepared to deal with these side-effects is that the area is woefully unstudied.
One of the early papers studying the effect of combination therapy with anti-CTLA-4 and GM-CSF on B16 melanoma in mice did note that: “After eradication of B16-BL6 tumors, 56% of the surviving mice developed depigmentation starting at the sites of vaccination and challenge and spreading to distant sites. Loss of coat color indicated that systemic and progressive autoimmunity had developed toward pigment-bearing cells”7. However, this side effect was overlooked in light of the major finding of the paper–that a tumorigenic, poorly immunogenic cancer could be eradicated in 80% of cases.
Indeed, eagerness to advance these exciting therapies from the bench to the clinic has outweighed the interest in studying potential side effects. Human trials are advancing faster than background research can be performed. In order to allow quicker access to life-saving drugs, the FDA has a “breakthrough therapy” designation, that allows faster approval of drugs8. Since 2012, the FDA has granted breakthrough designations 110 times, and about a quarter of these were approvals for immunotherapy drugs. Moreover, by and large, companies, physicians and patients consider the autoimmune side effects to be par for the course. Most patients don’t mind having to deal with diabetes, as long as their melanoma is cured. The problem with these rapid onset, unpredictable side-effects, however, is that they require constant vigilance. Additionally, without thorough background research, it is impossible to know the breadth of possible side-effects caused by these treatments. Further, the long-term impacts of such treatments are unknown. As such, while these checkpoint inhibitor treatments are a boon to cancer therapy, they must be approached cautiously and possible side-effects should be researched more thoroughly. If you should be interested in studying the side-effects of checkpoint inhibitor therapy, we carry GoInVivo™ anti-PD-1 and anti-CTLA-4 antibodies that are geared towards in vivo use in mouse models! Learn more with our webpage.
References
  1. Cancer: PD1 makes waves in anticancer immunotherapy.
  2. Immune System, Unleashed by Cancer Therapies, Can Attack Organs.
  3. Efficacy and safety of ipilimumab monotherapy in patients with pretreated advanced melanoma: a multicenter single-arm phase II study.
  4. Cutaneous, gastrointestinal, hepatic, endocrine, and renal side-effects of anti-PD-1 therapy.
  5. Nivolumab and ipilimumab versus ipilimumab in untreated melanoma.
  6. Anti-PD-1 and Anti-PDL-1 Monoclonal Antibodies Causing Type 1 Diabetes
  7. Combination Immunotherapy of B16 Melanoma Using Anti-Cytotoxic T Lymphocyte-Associated Antigen 4 (Ctla-4) and Granulocyte/Macrophage Colony-Stimulating Factor (Gm-Csf)-Producing Vaccines Induces Rejection of Subcutaneous and Metastatic Tumors Accompanied by Autoimmune Depigmentation
  8. Fact Sheet: Breakthrough Therapies
Contributed by Sarah Puhr, PhD.


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Blog - Tetramers - what are they and how can Flex-T™ help me with my research?

Comic by Pedromics.
Although they were developed 20 years ago1, Major Histocompatibility Complex (MHC) tetramers are only recently becoming widely available and easily accessible as tools for the study and characterization of antigen-specific T cells. Tetramers consist of soluble MHC proteins complexed with a peptide, and are an efficient and easy way to identify, isolate, and study antigen-specific T cells from a variety of biological samples. T cells, or T lymphocytes, are important players in the cell-mediated immune response, and are normally characterized by the presence of cell surface proteins such as CD4 or CD82. When exposed to certain stimuli, the T cells differentiate into particular subsets. One of these stimuli is an antigenic peptide that is presented to the T cell mostly by two classes of MHC. All nucleated cells have MHC-I molecules, while MHC-II molecules are usually only found on Antigen Presenting Cells (APCs).

We will only focus on class I and II for this blog, as they are the ones that mainly present peptides to T cells. The peptide-MHC complexes are recognized by the T Cell Receptor (TCR) and the CD co-receptor (CD4 or CD8). In order for the T cells to become activated, both the TCR and the CD co-receptor must bind to the peptide-MHC complex. The specificity of binding is conferred through the TCR; TCRs are specific to certain peptide sequences and therefore each T cell will recognize a unique peptide sequence that is associated with a particular pathogen. In a healthy person with a normal immune system, any pathogen that they have encountered in their lifetime will have activated a T cell with a TCR that is specific to a peptide that is present on that pathogen. These T cell clones then multiply in order to help get rid of the pathogen.
One property of the peptide-MHC complex that has made studying it so difficult is its low affinity for the TCR. This is necessary in order to allow each TCR molecule to bind multiple MHC-peptide complexes, and is the reason for the development of tetramers. When multimerized, the MHC complex/TCR interaction becomes more stable as the tetramer can bind multiple TCRs on the cell surface, in turn increasing the TCR binding affinity and decreasing the dissociation rate. So what exactly is a tetramer and how is it made?
At the heart of the tetramer is a fluorescently labeled streptavidin molecule which can bind four biotin molecules3. MHC tetramers are made of 4 biotinylated MHC complexes, loaded with the peptide of interest (8-10 amino acids for MHC-I; 14-20 amino acids for MHC-II)4. There are multiple ways to make these proteins – the most common is the enzymatic method. The heavy chain, the β2-microglobulin invariant light chain, the peptide, and the enzyme BirA are co-expressed in Escherichia coli and mixed together with the peptide. There is a 15 amino acid recognition tag expressed on the C-terminus of the MHC α-chain that allows the BirA enzyme to specifically biotinylate one lysine residue within the recognition tag. The monomers are then purified by size- and charge-exclusion chromatography, and the multimerization step happens upon the addition of streptavidin3. Since one streptavidin molecule can bind four biotins, the result is a tetramer. It is also possible to have multimers, depending on how many biotins the backbone of the multimer can bind.
If you are interested in a specific peptide, or want to use many different peptides, it’s possible to make the tetramers using an ultraviolet light photolabile peptide that can be displaced by the peptide of interest. This method allows for large-scale screening of any peptide of interest. BioLegend’s Flex-T™ MHC Tetramers offer the flexibility (see what we did there?) of loading any compatible peptide into the binding site of the complex, providing an affordable, easy way of studying antigen-specific T cells. You can learn more about the compatible antigen peptides here. If your peptide of interest is not listed, we also offer custom Flex-T™ monomer or tetramers – request yours here.
Now that you understand how the tetramers are made, you can probably think of many ways where this technology could be useful – and you would be right! Tetramers/multimers have been used by researchers to identify and quantify antigen-specific T cells from patient samples, which is especially useful when determining the effectiveness of a vaccine3. The frequency of CD8+ T cells can be assessed by enriching the sample for CD8+ T cells using a magnetic bead protocol, followed by staining with tetramers to identify a specific population and track the changes in that population over time. This can help understand disease progression as well as vaccine response, and can help inform doctors of how well the patient is responding to therapeutic intervention. Different tetramers can also be labeled with different fluorophores, allowing for a multicolor analysis to track multiple specificities of T cells from the same patient sample.
Possible combinations of two-color codes depend on the number of Streptavidin-fluorophore conjugates used to generate the tetramer/peptide complex.
It’s also possible to use tetramers to guide epitope mapping, more commonly used with MHC class II tetramers5. Instead of loading the MHC molecules with a specific peptide, they are loaded with a mixture of peptides from overlapping regions of the antigen of interest. These are then divided into pools of five to ten peptides and used to analyze cells that were stimulated with the antigen of interest. Once there is a positive stain, the individual peptides can then be loaded to identify T cells with a particular antigen specificity and MHC restriction. These cells can then be expanded in vitro and transferred back into the patient, as has been done for the treatment of HIV and cytomegalovirus (CMV) infections. All nine patients who received transplants of CMV-specific T cells showed a reduction in CMV viremia, with no observable side effects6. One patient had a chronic CMV infection that was refractory to treatment with antivirals but was controlled within 8 days of receiving the CMV-specific T cell transplant. It is important to be able to control CMV infection in immunocompromised patients, such as those with active HIV infection or cancer patients. Recently, dextramers were used to identify melanoma-specific CD8+ T cells from a solid tumor and from peripheral blood7. This study established the use of multimers in samples other than peripheral blood, and there are more similar studies underway across the world.
Tetramer assays have expanded the toolbox of researchers and physicians, allowing them to not only learn more about antigen-specific T cells, but about the immune response to pathogens and cancer in general. There is much more to learn about the immune system and how it interacts and responds to attack by foreign and self-associated antigens. Tetramers will continue to aid such discoveries and help to drive disease treatments in the future. Do you work with tetramers or have research you want to share with us? Get in touch with the Tech Team here!

References:
  1. Phenotypic analysis of antigen-specific T lymphocytes.
  2. Immunobiology, 5th edition
  3. MHC-peptide tetramers for the analysis of antigen-specific T cells.
  4. Unconventional recognition of peptides by T cells and the implications for autoimmunity.
  5. Tetramer-guided epitope mapping: rapid identification and characterization of immunodominant CD4+ T cell epitopes from complex antigens
  6. Adoptive transfer of cytomegalovirus-specific CTL to stem cell transplant patients after selection by HLA–peptide tetramers
  7. A novel MHC- dextramer assay to identify melanoma antigen-specific CD8+ T cells from solid tumor disaggregates and matched peripheral blood
Contributed by Rea Dabelic, PhD.


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Video - Awakening Oligodendrocyte Precursors: Recent Advances in Remyelination
Description: This video, provided by The Scientist, cosponsored by BioLegend, addresses the promotion of remyelination by resident oligodendricyte precursor cells and overcoming demyelination and hypomyelination.

Keywords: CNS, myelination, oligodendrocytes, neurons, neuroscience, OPCs, Oligodendrocyte precursor cells



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