immune system cell

i’ve seen a text post going around saying something to the effect of “do you know how much ur body loves you? so you should love it back!” (i’m paraphrasing here)

i want to give a shoutout to girls with autoimmune illnesses.

to the girls whose bodies don’t love them, to the girls whose bodies betray them every instant of the day, to girls whose immune system attacks the very cells it’s designed to protect:

i love you and i am so, so sorry that you are in this position. i wish i could offer advice or make it go away but i can’t.

for me, one of the worst things about being diagnosed w/rheumatoid arthritis was the loss of confidence that went with it because i started thinking “why bother loving my body if it doesn’t even love me?”

i still don’t know, intellectually, why you should love your body but i know that learning to love it again was the best decision i ever made (tho god knows i’m forever a bitter cripple). 

please remember that it’s okay to mourn the life your disability didn’t let you have. but one day, i hope that every girl with an autoimmune illness can learn protect and love her body even though it doesn’t love her back.

i’m still trying to learn too.

Passive Immunotherapy

Active immunotherapies:

  • Cytokines (TNFa IL-2, IFNs)
  • Cancer vaccines
  • tumour CTL and APC
  • DC priming

Passive immunotherapy:

  • Administration of monocolnal (clone derived asexually from a single individual or cell) antibodies which target either tumour-specific or over expressed antigens
  • Generally comprised of antibodies made outside of the body (in a lab)
  • administered to patients to provide immunity against a disease, or to help fight existing disease
  • do not stimulate a patient’s body to ‘actively’ respond to a disease the way a vaccine does
  • immunogen is given several times to induce a strong secondary response
  • blood serum contains many different antibodies to the immunogen
  • most immunogens have multiple antigenic epitopes 
  • each stimulates a different B cell clone/receptor –> polyclonal antibody (PAb) response 

Monoclonal antibody (mAb) therapy is the most widely used form of cancer immunotherapy. Monoclonal antibodies cannot be purified from a polyclonal sample and are derived from a single clone/specific for a single epitope.

Antibodies in cancer therapy:

  • Trigger immune system to attack cancer cells 
  • Block molecules that stop the immune system working (checkpoint inhibitors)
  •  Block signals telling cancer cells to divide 
  • Carry drugs or radiation to cancer cells

Checkpoint inhibitors

  • Immune system uses particular molecules to stop it being over activated and damaging healthy cells  - these are known as checkpoints
  • some cancers make high levels of checkpoint molecules to switch of immune system T cells which would normally attack cancer cells
  • examples of targets include CTLA-4, PD-1 and PD-L1 (programmed death ligand 1)

Blocking cell division signals 

  • Cancer cells often express large amounts of growth factor receptors on their surface –> rapid cell division when growth factors stimulate them
  • some monoclonal antibodies stop growth factor receptors working
  • either by blocking the signal or the receptor itself 
  • cancer no longer gets signal to divide

Carrying drugs/radiation

  • drugs or radioisotopes can be attached to monoclonal antibodies
  • the mAB binds to the cancer cell, delivering directly
  • known as conjugated MABs

Cellules du système immunologique : cellules qui combattent les maladies dans le corps ou pathogènes.

  • n°1 : Phagocyte en phase d’endocytose du pathogène. La cellule peut capter les virus ou les bactéries, les enveloppe avec deux bras - les pseudopodes - pour l’inclure en son sein : c’est l’endocytose. L’intrus est ensuite digéré par les sucs contenus dans des petites vésicules.
  • n°3 : Lymphocytes T cytotoxiques. Ils sont spécifiques, c’est à dire que chaque type de lymphocyte ne peut tuer qu’un type de pathogène. Les cytotoxiques éliminent les cellules infectées qui circulent dans le sang en les faisant exploser de l’intérieur avec des enzymes : c’est la cytolyse.
  • n°5 : Rien à voir avec l’immunologie, les hématies ou globules rouges circulent dans le sang et transportent l’oxygène nécessaire au fonctionnement des organes.
  • n°7 : Monocytes : voyagent dans le sang. Si le corps détecte une infection, les monocytes sortent des vaisseaux et se transforment en macrophages, des cellules capables de phagocyter les agents infectieux (voir n°1).
  • n°9 : Granulocytes : cellules capables de phagocytose aussi. Contient des granules digestives. A la particularité d’avoir un noyau en plusieurs lobes, donc aussi appelé polynucléaire - à tort.
  • n°11 : Lymphocyte B. Cellule spécifique qui peut se transformer si besoin en “usine” à anticorps.

Mitose : processus de duplication de la cellule en conservant le patrimoine génétique intacte de la cellule mère.

  • n°2 : cellule normale, avec membrane, noyau et cytoplasme. La base!
  • n°6 : Interphase. Phase ou la cellule grossie avant de se séparer en deux, et ses chromosomes se multiplient par deux.
  • n°4 : Prophase. Les parois du noyau éclate, et les chromosomes deviennent visibles au microscope.
  • n°10 : Métaphase : Les chromosomes se placent en centre de la cellule.
  • n°8 : Anaphase : Ils migrent ensuite aux pôles de la cellule de façon symétrique : on retrouve les mêmes chromosomes de part et d’autres de la cellule.
  • n°12 : Télophase : La cellule se sépare en deux et l’enveloppe du noyau se reforme sur les deux ensembles de chromosomes pour avoir deux cellules identiques.

J’adooore la biologie!

ELI5: Getting sick from a 'bacteria' vs. 'virus'

Bacteria produce harmful chemicals as part of their life processes. They use up your body’s resources (like eating your sugar or even eating your cells) and spit out toxic waste. Sometimes that waste is specifically designed to protect the bacteria by killing your immune system cells that try to attack it. But it also just basically poops all up in your body, which causes some damage. The symptoms of bacterial infections are related to what waste products the bacteria produces and where the bacteria is living. Your body fights bacterial infections by basically eating them, along with some other toxic chemicals that destroy them.

Viruses hijack the DNA in your cells to make more of the virus. They invade the cell and tell it to stop doing whatever it’s doing that your body needs it to do, and instead all it does is manufacture more of that virus. Eventually, the cell dies - usually by literally exploding - when it fills up with copies of the virus. Those viruses go on to infect other cells. Viral symptoms are caused by your body’s own attempt to kill them, and by the deaths of the cells they’re infecting. Your body fights viruses also by eating them, but it’s harder because they’re a lot smaller and have special protein shells that disguise them as “totally not a virus don’t eat me you guys”.

For extra fun, there are also prion diseases! Prions are proteins that folded the wrong way. When properly-folded proteins come into contact with prions, they re-fold into the same wrong shape as the prion. Your body can’t do anything about it because although it’s folded wrong, it’s still a protein that’s supposed to be there. Proteins are the way your body communicates and accomplishes certain things, so folding them wrong can really muck-up what is supposed to happen. In the case of Mad Cow Disease, as more and more proteins turn into prions, your brain turns to mush and gets holes in it until you go crazy and die.

If you think of your body as a factory that builds cars: bacteria are like a drunk hobo sneaking into your factory and dumping empty wine bottles into the machinery so it breaks. Viruses are like a roomba wandered in and reprogrammed your factory to start making more factory-invading roombas instead of cars. Prions are like a weird European car showed up and crashed into one of your factory’s cars after it left the factory, and now they both keep crashing into other cars (which then go on to crash into more cars) and also they all keep crashing into your factory.

Also fungal infections. Fungi can’t produce their own food, so they steal yours. Often that means invading parts of your body to get to it, and dumping toxic waste like bacteria. In the factory, a fungus would be someone building a shed attached to your factory and stealing your power so your factory doesn’t have enough to run and dumping garbage into your factory.

Also also, parasites. Parasites do the same thing as bacteria, but they’re [often] multicellular, so they’re much larger. Instead of a bunch of them, it’s usually a few big ones (although sometimes also a lot of them). In the factory, a parasite would be like the mafia moving into your factory, breaking stuff, and punching you right in the kidneys (or more likely, in the intestines) while they steal your money.

Explain Like I`m Five: good questions, best answers.

Diabetes: Type 1 vs Type 2

TYPE 1

Total lack of insulin

  •  5 to 10% of people who have diabetes.
  • autoimmune disease - immune system attacks beta cells in pancreas that produce insulin
  • eventually eliminating insulin production from the body.
  • cells cannot absorb glucose to produce energy
  • symptoms usually start in childhood or young adulthood. 
  • episodes of low blood sugar level (hypoglycemia) are common
  • cannot be prevented  
  • treated with insulin injections or pump

TYPE 2

 Too little insulin or cannot use insulin effectively 

  •  can develop at any age but most commonly becomes apparent during adulthood. 
  • vast majority of diabetics
  • body develops insulin resistance 
  • body compensates by producing much more, but can’t always produce enough and eventually beta cells may be destroyed from overwork - resulting in deficiency 
  • may not have symptoms before diagnosis
  • there are no episodes of low blood sugar level, unless the person is taking insulin or certain diabetes medicines.
  • can be prevented or delayed with a healthy lifestyle 

Both types increase a person’s risk for complications. Diabetes is the leading cause of blindness and kidney failure.

  • excessive build up of blood glucose causes an increase in osmotic pressure 
  • the kidneys no longer able to absorb most of the glucose - due to extreme concentration
  • the body pulls fluid from the tissues to try to dilute the blood and counteract the high glucose 
  • dehydrated tissues signal the need to drink more, subsequent increase in urination 
bbc.com
Immunotherapy cancer drug hailed as 'game changer'
Immunotherapy works by harnessing the immune system to destroy cancer cells.

An immunotherapy drug has been described as a potential “game-changer” in promising results presented at the European Cancer Congress.

In a study of head and neck cancer, more patients taking nivolumab survived for longer compared with those who were treated with chemotherapy.

In another study, combining nivolumab with another drug shrank tumours in advanced kidney cancer patients.

Immunotherapy works by harnessing the immune system to destroy cancer cells.

Advanced head and neck cancer has very poor survival rates.

In a trial of more than 350 patients, published in the New England Journal of Medicine, 36% treated with the immunotherapy drug nivolumab were alive after one year compared with 17% who received chemotherapy.

Patients also experienced fewer side effects from immunotherapy.

Continue Reading.

‘Serial Killers’ Seek Out & Destroy Cancer Cells In Astonishing New Video

“Inside all of us lurks an army of serial killers whose primary function is to kill again and again."That might sound like something you’d hear in a movie preview. In fact, it’s Prof. Gillian Griffiths, director of the Cambridge Institute for Medical Research in England, and she’s talking not about science fiction but about a very real kind of immune system cell.

does anyone recall when Maria hill mentioned that Pietro has an increased metabolism?

if I’m not mistaken, that means he wouldn’t just be able to run at incredibly high speeds. all of his bodily systems would have to function at incredibly high rates, especially if his body is going to handle and support such a fast runner. Everything from his muscles to his nerves to his respiratory system would have to work much faster than normal. his heart would beat very very fast, which would pump his blood pretty quick too, which leads me to believe that if he were wounded, say, a bullet to the arm, Pietro would probably bleed quite a bit.

But remember, he has an increased metabolism.

Meaning his immune system and white blood cells would also work much faster than normal, which only tells me that not only can he run fast, but he can also HEAL pretty fast too.

This explains why when he’s shot in the arm, he doesn’t really show any signs of actual pain, and the wound doesn’t look like it bleeds much for a bullet wound. Most likely, as soon as he took off again after being shot the first time, his arm was probably pretty well healed over.

And the point? Well, when Ultron shot at Clint and Pietro took the bullets, of course the caliber and speed of the bullets was greater, not to mention the number. So yeah, he took extensive damage, and maybe was dead for a few minutes at most, but most likely, by the very end of AOU, the only reason we don’t see him in the new Avengers line up is because Wanda grounded him to his hospital bed for scaring her so bad.

Connecting Alzheimer's disease and the immune system

The role of the immune system in Alzheimer’s disease is a hot topic, but exactly how the two are connected and what interventions could help lower risk remain a mystery. In a new study published in Nature Neuroscience, researchers in the Ann Romney Center for Neurologic Diseases at Brigham and Women’s Hospital (BWH) investigate how genetic risk factors for Alzheimer’s disease may influence a key type of immune cell. Their results lay the groundwork for designing better therapeutic strategies and better prediction tools for risk of developing Alzheimer’s disease.

“There’s an emerging theme in Alzheimer’s genetics that the immune system may be strongly involved in the onset of Alzheimer’s disease,” said co-corresponding author Philip De Jager, MD, PhD, who directs the Program in Translational NeuroPsychiatric Genomics at the Ann Romney Center for Neurologic Diseases at BWH. “Before genetic studies, many thought that inflammation was a symptom of or a reaction to the disease, but our study and others build a compelling case that the immune system may be involved in the development of Alzheimer’s disease.”  

De Jager and his team examined the levels of key proteins in relation to genetic variants that have been implicated in Alzheimer’s disease in the past. The team looked at blood samples from more than 100 younger, healthy subjects as well as 61 older subjects and measured protein levels in monocytes - immune cells that can travel to various sites throughout the body, including the brain where they differentiate into macrophages, specialized for their new environment, in this case the central nervous system.

One of the most intriguing results the team uncovered is connected to TREM2 - a protein that is a major target of Alzheimer’s disease drug development efforts. A previous study of a population in Iceland found that a rare mutation in the gene encoding TREM2 substantially elevated a person’s risk of Alzheimer’s disease. However, it was unclear whether more TREM2 or less TREM2 led to this heightened risk, and follow-up studies in mice have produced conflicting results.

De Jager and his colleagues found evidence that directly addresses this question, determining that higher levels of TREM2 were associated with increased risk. The team found that a genetic variant tied to a separate protein, CD33, also influenced TREM2 levels. The team’s follow-up studies confirmed that the genetic variant led to more CD33, which in turn led to more TREM2. “One interesting note about these protein associations is that we did not observe them at the mRNA level,” said first author Gail Chan, PhD, a research fellow in the Ann Romney Center for Neurologic Diseases at BWH. “This emphasizes the amount of inter-regulation that a cell does to balance all of the related molecules in order to function correctly.”

“Up until now, it’s been unclear whether it would be beneficial to increase or decrease TREM2 levels,” said co-corresponding author Elizabeth Bradshaw, PhD, of the Ann Romney Center for Neurologic Diseases at BWH. “Further studies are needed to understand the connections we’re uncovering and the roles of these proteins, but we’re clearly seeing evidence that these genetic variants have an effect in this type of immune cell.”

As a next step, Bradshaw, De Jager and their colleagues plan to measure CD33 and TREM2 levels in subjects as part of the Brigham Healthy Aging Project to determine if these measurements and others could be part of a diagnostic panel for predicting risk of Alzheimer’s disease.

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April 17th is No Shame Day. A day where people like me can talk openly about their disabilities. My name is Brenna and I have Crohns Disease. It’s been 5 years and a crazy journey that started during my freshman year of high school. Crohns is an irritable bowel disease that can affect the entire digestive system. It’s an autoimmune disease where your immune system mistakes your cells for foreign invaders thus causing massive amounts of inflammation and pain. My disease is primarily in my ileum in my small intestine. I now have a build up of inflamed scar tissue, called a stricture, in my intestine so thick that a colonoscopy camera can’t push past it to get a better visual on the rest of my system. I was on remicade for 4 years, until I grew immune and now I’m unmedicated and scared. I worry daily about hospitalization and medical bills. Living this way, I forget almost what it was like pre-disease. I get infections at an alarmingly easy rate because of the immunosuppressive drugs. It makes things like getting my nails done difficult. My weight is all over the place as steroids make me gain and sickness makes me shed all my healthy weight. My skin is definitely changed. I break out and react to things more often, I can also no longer tan as remicade has made me increasingly photosensitive. This disease at times embarrasses me. Makes me feel ugly, unworthy, and like I’m complaining about stuff that doesn’t matter. Some days I feel like I should just “get over it” and push through it like a healthy person. Then the next, I’m in the hospital for a serious obstruction. Many people will look at me and say I’m healthy, but invisible diseases matter. My pain is real and my struggle is real. I used to feel like if I didn’t give off the appearance of a healthy person, no one could love me. Today, I have a fiancé who loves me more than I think I’m worthy of, crohns and all. I’m in college online because it works with my schedule and between my symptoms. One day, I know I’ll find remission and the daily pain will stop. Until then, I’m beautiful and I can take on the world one step at a time.