From what I know, IgE attaches to Basophils and Mast Cells to release Histamine, which then activates an allergic reaction, but I am not sure why is it so easy to induce an allergic reaction, when the adaptive immune system takes a few days to do the Cloning Selection, is it because memory cells stay?
Extra Question: Does IgE also attach to Eosinophils for parasitic attacks? If so, what does it accomplish by attaching to it?
Wouldn't the first dose result in memory B cells after doing the germinal center/recombination/immunoglobulin class switching stuff? If no memory cells occur after the first dose, it would be as if it never happened. But if memory cells exist after first dose, why are subsequent doses necessary?
Hi there, I am a first year dental student and I was wondering if anyone could help me to better understand all of the underlying reasons of why we need to prevent gingivitis in the management of periodontal disease. My understanding is that periodontal disease is a progression of gingivitis that results in bone attachment loss, so in this sense it would make sense to prevent the ‘precursor’ which is gingivitis in this case.
I’m not sure if my understanding is correct and I think I might be missing something. I’m also not sure how the innate/adaptive immune system ties into this exactly.
It would be cool if I could get a slightly better understanding through you guys and use that to guide my further research into academic papers/textbooks. Cheers!
My understanding is that essentially every virus capable of causing an infection in a human has some means of messing with the innate immune system so as not to immediately be wiped out by it. But how common is it for viruses to have non-structural proteins in their genome that are targeted at messing with the adaptive immune system?
Hi all! I was just summarizing my notes and trying to make connections on the immune system - something I tend to get super confused about. I've made a comprehensive and easy to follow list so I thought I would share it with anyone who may be struggling with the immune system and for those who feel like there may be some corrections to be made. Let me know!
Immune system is divided into:
- Innate immune system - non specific such as leukocytes (neutrophils, basophils, eiosinophils, NK cells), macrophages, phagocytes etc.
- Adaptive immune system - specific such as B cells (humoral immunity) and T cells (cell mediated immunity)
T cells are divided into two kinds:
- effector T cells - further divided into helper T cells (CD4) and cytotoxic/killer T cells (CD8)
- memory T cells - act similar to memory B cells which are extra prepared when the foreign pathogen strikes another time and elicit a quicker response
- suppressor T cells - carry out negative selection to destroy the cells that are responsible for autoimmune diseases because they attack cells of the body aka the self.
When the T cells are presented with an antigen presenting cell (which can be a B cell, or a macrophage, or a dendritic cell) it will divide into specific effector T cells or memory T cells.
The helper T cells (CD4) will recognize the antigen on the MHC II (major histocompatibility complex II) and cause proliferation of B cells into:
- Plasma B cells: that produce antibodies
- Memory B cells: that prepare the body better if the foreign pathogen strikes again
The helper T cell will also cause other cells of the immune system to activate but it will itself not release any cytokines to destroy the foreign pathogen.
The cytotoxic T cells (CD8) however respond to MHCI and will release toxic chemicals if they come in contact with the pathogen.
The antibodies produced by the plasma B cells further can carry out three mechanisms:
- opsonization (tagging) of the pathogen for easy destruction by the rest of the immune system
- clumping the pathogen together for easy phagocytosis by macrophages
- inactivating the pathogen altogether so that it is unable to invade any tissues.
I'm using the 2019-2020 kaplan books. Interferons and MHC complexes are discussed under the innate immune system section, but surely these ideas are not exclusive to the innate immune system, right? CD4 cells (helper T cells) respond to MHCII and can alert both the innate and adaptive immune system, while interferons upregulate MHC presentation. Therefore interferons should be associated with both systems too. Any pointers would be greatly appreciated.
Does HIV attack b cells? And does B cells have TLRs? If so what type of TLR do they have?
The same question goes with Natural Killer cells, Does HIV attack natural killer cells? And do they have TLRs? If so what type of TLR do they have?
The Hypothalamic–Pituitary–Adrenal (HPA) axis stimulates and depresses various parts of the immune system at different hours of the circadian day as determined by the body's central clock in the suprachiasmatic nucleus (SCN). If, e.g., your daily waking and eating times are begin when the SCN still thinks it's night, can the peripheral clocks that govern the immune system entrain to a different rhythm than the HPA's rhythm of cortisol release? If so, how could someone determine if that had occurred in their own case?
Specifically the presence of innate vs adaptive in insects and humans. Thanks!
I'm a relatively new professor of microbiology at a nursing school. My students are new to science, and many have never taken a biology class. I'm currently trying to explain how the immune system works. I know I've grossly simplified, but I'm hoping I did a good job explaining the roles well, and reasonably succinctly. Thoughts?
How the immune system is just like a zombie apocalypse scenario:
Think of a human body as a camp of survivors of a zombie apocalypse. The zombies are outside, trying to get in, but sometimes it's hard to tell who is a normal person inside the camp, and who is a zombie.
So, a virus infecting cell makes it a zombie, right? A cytotoxic T-cell is like a police officer who can look at someone and see if they've been bitten by a zombie. The cytotoxic T-cells go around looking at the "normal" body cells to see they're doing anything weird. Normal cells are wearing a uniform called MHC-Class One. That uniform says "I'm a civilian and I belong here". If a civilian cell is behaving strangely, though, the police man tells it to kill itself before the rest of the cells become zombies, too. The police T-cell knows that if one person is acting strangely, there are probably more that were bitten by zombies - so it makes lots of copies of itself and all the police go through the camp searching for people bitten by zombies and helping each infected person (virus infected cell) kill itself.
An antibody is like a dog trained to sniff out zombies. It doesn't kill them, but it can stick to the zombies and tell the soldiers where the zombies are. The B-cells are like the trainers that train the zombie-sniffing dogs. If a trainer spots a zombie, it will first make a bunch of other trainers (plasma cells), and then all the trainers will start training zombie-sniffing dogs (antibodies) that fan out all over the camp to find the zombies. The trainers never forget the zombie, so even after all the zombies in one attack have been killed, they'll be ready at a moment's notice to train some new zombie-sniffing dogs.
The soldiers are the macrophages. They wander the camp and catch anything foreign. If they see a zombie-sniffing dog has cornered something, they will rush to attack. They can also pick out some really obvious zombie characteristics (the smell of rotting flesh, moaning for brains) and attack the obvious zombies (macrophages "smell" danger - like peptidoglycan - using Toll-Like Receptors).
The soldiers are not very smart,
... keep reading on reddit ➡So I was reading that our immune system with MHC (or HLA) molecules evolved in vertebrates. MHC molecules are the main locus of genetic diversity in disease resistance in humans, do wildplants have any similar region with lots of diversity, and if not why is it frequently asserted that monocultures may be more susceptible to disease?
