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A group of University of Pittsburgh researchers has given new meaning to "knowing your ABCs."
Rituxan postponement
Today I am getting blood work done. My specialist wants to see a few things. First, my B cell counts. With the hundreds of blood tests I’ve had done in the hospital, that wasn’t done. There was no need to break out the specific white blood cells for a pneumonia. The second thing is my immunoglobulin blood test. I was running very low in the hospital throughout the few months. The pneumonia…
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First Kesimpta dosing shot
First Kesimpta dosing shot
I started getting freaked out reading other people’s first shot reactions on the Facebook Kesimpta group. I thank Sherry for commenting on my Kesimpta delivery blog and telling me about the group but it didn’t help my nerves. Thankfully, I had a video conference with my neurologist yesterday. She explained Kesimpta is nothing like the interferon shots that I took for the first 12 years. The shots…
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Cancer drugs shed light on rheumatism
Cancer drugs shed light on rheumatism
Cancer drugs shed light on rheumatism
Reporter: Irina Robu, PhD
The human body is often described as being ‘at war’. By this, it is meant that the body is constantly under attack from things that are trying to do it harm. These include toxins, bacteria, fungi, parasites and viruses. The human immune system is one of the most effective defense mechanisms known to nature and can sometimes can be…
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New Multiple Sclerosis Culprit Identified-B-cells and T-cells in MS Medical News Today
New Multiple Sclerosis Culprit Identified-B-cells and T-cells in MS Medical News Today
https://www.medicalnewstoday.com/articles/323006.php
New multiple sclerosis culprit identified
It is still unclear what causes multiple sclerosis, but new research closes in on the faulty immune system mechanisms involved in the development of this condition.
New research has identified another type of immune cell that may play a role in MS.
Multiple sclerosis(MS), which is an autoimmune…
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April was Primary Immunodeficiency Awareness Month, but I was so overwhelmed with crazy end-of-semester stuff and crazy body stuff that I totally goofed—I didn’t write a single PI awareness post on my blog about PI. But better late than never right? So let’s talk about it. What is a primary immunodeficiency and what is it not?
What PI is:
A hereditary/genetic defect in the immune system.
A defect occurring in one or more components of the immune system.
A blanket term to describe more than 350 rare, chronic disorders in which part of the immune system is missing or functioning improperly.
Lifelong.
Treatable, but not curable.
Basically a primary immunodeficiency is a problem with your immune system that you’re born with (although they can develop later in life and often aren’t diagnosed for many years either way).
What PI is not:
Contagious.
An autoimmune disorder.
Just a “bad” immune system.
Visible.
A defect in the immune system caused by something else—like AIDS or chemotherapy (it’s not “acquired”).
So when someone tells you they have PI don’t get all weird about it. They’re not contagious. Most likely, they’re not dying. Just be cool.
What having PI means:
Increased susceptibility to contagious illnesses.
Increased susceptibility to infection.
Infections that are recurring, chronic, difficult to clear up, severe, or caused by unusual organisms.
You don’t build immunity from a previous infection (whether viral or bacterial).
You’re a medical zebra—PI is rare, so it’s a “zebra” condition instead of a more common “horse” condition.
Let me explain—no there’s too much. Let me sum up. Having a primary immunodeficiency means you get sick a lot, because your immune system doesn’t work like it should. Since it’s a genetic/hereditary disorder, having PI usually means it either runs in your family, or you’re really lucky and your genes mutated…
To better understand PI it’s important to understand how the immune system is supposed to work
How it Works – The Immune System
There’s two basic parts to the immune system: the innate immune system and the adaptive immune system.
The Innate immune system starts, like all of the cells that make up the immune system, in the bone marrow with a stem cell. The several types of cells that make up the innate immune response (neutrophils, monocytes, natural killer (NK) cells, complement proteins) are ready to go straight to work once formed. They require no additional training to do their jobs.
In most cases of PI the innate immune response is a-okay. The problem occurs in the adaptive immune response.
The Adaptive immune system also starts in the bone marrow. There they become either B-cells or T-cells, the two major parts of the adaptive immune sytem. Then they are split up. T-cells go to the Thymus to finish developing and get trained for their jobs as Killer T-cells, Helper T-cells, or Regulatory T-cells—which all basically deal with the body’s adaptive response to foreign substances (ie viruses) and make sure they don’t attack the body’s own tissues (as in autoimmune conditions).
B-cells stay behind and get edumacated in the bone marrow. They mature into Plasma cells, which in turn can mature further into Memory B-cells. Plasma cells are responsible for producing antibodies, which are highly specialized proteins that fit “invaders” like a key in a lock. Memory B-cells remember the invaders that you’ve encountered before so a rapid response can be mounted if you encounter it again.
In a lot of primary immunodeficiencies the main problem is with the B-cells. They don’t mature like they’re supposed to. They don’t pay attention in bone marrow class or just skip it all together. So they don’t make antibodies like they should and they definitely don’t remember past infections. It’s like your adaptive immune army is made up of a bunch of cats—they just do whatever the heck they want, which is usually nothing. So bacteria and viruses waltz in again and again, and even if they’ve gotten in before your cells are perpetually unprepared.
Basically your B-cells look like this:
So you can see why they might not be super effective…
What is Primary Immunodeficiency? April was Primary Immunodeficiency Awareness Month, but I was so overwhelmed with crazy end-of-semester stuff and crazy body stuff that I totally goofed—I didn’t write a single PI awareness post on my blog…
Naive and memory B cells On a side note, a little change of style in comics. Hope you like it!
Regulatory B-cells play an important role in immune response and inflammatory reaction
http://www.cusabio.com/Polyclonal-Antibody/Rabbit-anti-human-Cellular-tumor-antigen-p53-polyclonal-Antibody-11106204.html
B-cells play role of immune regulation mainly by presenting antigen and producing antibodies. In recent years, it was found that part of the B-cells play regulatory role in immune response and inflammatory reactions. These B-cells are named regulatory B-cells. Regulatory B-cells can produce IL-10 to reduce inflammation, controlling T-cell immunity.
Research team from school of Life Science at Sun Yat-sen University found cancer-promoting regulatory B-cells in human hepatocellular carcinoma. The results were published recently in the journal Cancer Discovery and the article corresponding author is Professor Kuang Dong Ming from School of Life Sciences.
Studies have shown that B-cells promote tumor development continued to express higher levels of PD-1 (programmed cell death-1), in advanced hepatocellular carcinoma (HCC) accounts for 10% of all B cells. Hepatocellular cancer is one of the highest of the main types of primary liver cancer, but also the degree of malignancy.
Further studies showed that, TLR4-mediated upregulation of Bcl-6 cells for induction of HCC environment B is very important. PD-1 expression in B cells by IL-10 signal, inhibition of tumor-specific T cell immunity; promote the development of hepatocellular carcinoma.
Nicotinamide ribose (nicotinamide riboside) is a derivative of vitamin B3. Scientists have recently discovered that this substance through dietary supplements, can prevent the development of liver cancer in mice, and induce tumor regression. Spanish National Cancer Research Centre (CNIO) researchers, the establishment of the first truly reproduce HCC development in a mouse model. Studies have shown that DNA damage in the early stages of HCC, nicotinamide ribose rich diet can provide protection for the mouse.
Cyclin cyclin E1 cell cycle G1 / S transition when a key regulator of hepatocellular carcinoma and other cancers. Despite the expression and regulation of cyclin E1 stability it has a better understanding, but it is unclear post-transcriptional regulation. To this end, Fudan University researchers conducted in-depth research. They found that, HCC samples ubiquitous nuclear factor 90 (NF90) of the regulation, NF90 is a double-stranded RNA binding protein. Studies have shown, NF90 by regulating cyclin E1 mRNA stability, cell cycle control of HCC. NF90 can reduce cancer cell growth inhibition, delaying G1 / S transition.
Hypoxic microenvironment invasion and metastasis of HCC is a powerful driving force. As we all know, HIF-1α (hypoxia inducible factor) is a key transcriptional regulator of hypoxic response, capable of inducing the expression of multiple target genes involved in different stages of HCC metastasis. HCC metastasis essential molecular mechanism for understanding these target genes identified. Research team at Fudan University and Shanghai Jiaotong University identified an important target gene of HIF-1α in HCC, providing a potential new target of HCC treatment.
