innate immune system

All about closed comedones

What are closed comedones?

A comedo (the singular form) is a clogged hair follicle (pore) in the skin. Keratin (skin debris) combines with oil to block the follicle. A comedo can be open (blackhead) or closed by skin (whitehead), and occur with or without acne. But when most people refer to closed comedones they are references bumps like the one in the image. Non inflamed, skin coloured bumps, often found on the forehead.

Caused of closed comedones

There are many causes. Pro-inflammatory cytokines (cell signalling proteins), produced by cells lining the follicle in response to activation of the innate immune system. Free fatty acids made from sebum by acne bacteria
Overhydrated skin premenstrually, from moisturisers or in humid conditions
Contact with certain chemicals including oily pomades, isopropyl myristate, propylene glycol and some dyes in cosmetics. Rupture of the follicle by injury such as squeezing pimples, abrasive washing, chemical peels or laser treatments. Smoking – comedonal acne is more common in smokers than in non-smokers. Certain dietary factors may contribute to comedonal acne, particularly milk products and high glycaemic-index foods (sugars and fats).

How to treat from the inside out

- Stop smoking if you smoke.

- Reduce the processed sugars in your diet.

- Increase consumption of anti inflammatory foods such a leafy green veggies.

- Attampt to cut out dairy from your diet.

- Ensure you stay hydrated, drinking at least 2 litres a day so that you aren’t relying on heavy moisturisers.

How to treat with skincare products

Apply one of these once or twice a day as a thin layer.

Benzoyl peroxide
Azelaic acid
Salicylic acid
Glycolic acid

If your comedonal acne persists seek advice from your doctor or dermatologist.

Hope this helps you guys! Keep treating yo skin right

theamazingz  asked:

so what exactly does a space biologist do??

Hi! So my particular research will be essentially trying to figure out why astronauts get sick in space. I’m using fruit flies as a model to study the human innate immune system, so I’ll be sending a bunch of fruit flies to the space station and looking at their ability to survive infection once we bring them back. I’ll also be studying how being in space affects bacteria, since we know that microgravity causes changes to pathogens as well (it makes them more lethal). Since we will hopefully be sending people to Mars soon, it’s important to make sure that we can protect our bodies from the harsh effects of long-term space travel!

Great Immunology Videos 

Immunology Overview 

Innate Immune System

Adaptive Immune System 

Immune Cell Map 1 - Immune Cells 

Immune Cell Map 2 - Organs and Tissues

Immune Cell Map 3 - T cells part 1

Immune Cell Map 4 - T cells part 2

For More Great video review click Here! he has great reviews on all systems and subject needed for MCAT Biology Section!

And Check my Archive for my Previous review! 

Migrating immune cells promote nerve cell demise in the brain

The slow death of dopamine-producing nerve cells in a certain region of the brain is the principal cause underlying Parkinson’s disease. In mice, it is possible to simulate the symptoms of this disease using a substance that selectively kills dopamine-producing neurons. Scientists from the German Cancer Research Center (DKFZ) have now shown for the first time in mouse experiments that after this treatment, cells of the peripheral immune system migrate from the bloodstream into the brain, where they play a major role in the death of neurons. The investigators were able to reduce the level of neurodegeneration using a substance that blocks a specific surface molecule on these inflammatory cells.

A small area in the midbrain known as the substantia nigra is the control center for all bodily movement. Increasing loss of dopamine-generating neurons in this part of the brain therefore leads to the main symptoms of Parkinson’s disease – slowness of movement, rigidity and shaking.

In recent years, there has been increasing scientific evidence suggesting that inflammatory changes in the brain play a major role in Parkinson’s. So far, it has been largely unclear whether this inflammation arises inside the brain itself or whether cells of the innate immune system that enter the brain from the bloodstream are also involved.

At the DKFZ, a team led by Prof. Dr. Ana Martin-Villalba is investigating causes of cell death in the central nervous system. Neuroscientist Martin-Villalba has suspected that a specific pair of molecules, the CD95 system, is involved in neuronal death in Parkinson’s. This pair consists of the CD95 ligand and its corresponding receptor, CD95, also known as the “death receptor”.

Martin-Villalba recently showed that after spinal cord injury, inflammatory cells use these molecules to migrate to the injury site, where they cause damage to the tissue. Martin-Villalba then wanted to investigate whether peripheral inflammatory cells also play a role in chronic neurodegenerative processes such as Parkinson’s disease.

To investigate the process of neurodegeneration in mice, the scientists utilized a model system using the substance MPTP, which causes the selective death of dopamine-generating neurons in the human brain. In mice, MPTP typically causes Parkinson-like symptoms.

However, in mice whose inflammatory cells (monocytes, microglia) were unable to produce CD95L, MPTP treatment resulted in almost no neurodegeneration. This suggested that CD95L-bearing inflammatory cells are involved in the destruction of neurons. However, it remained unclear whether the true culprits are specific macrophages in the brain called microglia, or rather monocytes in the bloodstream that infiltrate the brain.

In order to make this distinction, the investigators used a chemical that blocks CD95L without being able to pass the blood-brain barrier. This substance therefore reaches only the inflammatory cells that circulate in the bloodstream and not the microglia that reside in the brain. Mice that had received this substance were also protected from MPTP-induced neurodegeneration.

“Thus, we have shown for the first time that peripheral inflammatory cells of the innate immune system also play a role in neurodegeneration,” say Liang Gao and David Brenner, first authors of the publication. “A key role in this process is played by CD95L, which enhances the mobility of these cells.”

Project leader Martin-Villalba speculates that a self-reinforcing vicious cycle arises in the brain: The breakdown of a few neurons that die from various causes attracts inflammatory cells that, in turn, further fuel the death of more neurons through inflammation-promoting signaling molecules.

At present, the researchers can only indirectly conclude that the results obtained in the artificial animal model are also relevant in human Parkinson’s disease. In collaboration with colleagues from Ulm, Martin-Villalba’s team recently found elevated quantities of inflammatory monocytes that were hyperactive in blood samples from Parkinson’s patients. Monocyte number correlated with the severity of disease symptoms. However, the researchers do not yet know whether these inflammatory cells also migrate into the brains of patients and contribute to the demise of neurons there, like they do in the mice with Parkinson’s.

“If this is the case, drugs that inhibit CD95L might mitigate Parkinson’s symptoms if administered early on – similar to what we observed in our experimental mice,” says Martin-Villalba. The substance required for this has already been investigated in clinical Phase II trials. Martin-Villalba also suspects that activated cells of the peripheral immune system might drive neurodegeneration not only in Parkinson’s disease but also in other neurodegenerative disorders such as Alzheimer’s.

Innate Response to Viral Infection

A viral infection is detected by changes in MHC levels on infected cells as well as activation of TLR3 by dsRNA.

All cells in general…

  1. Are alerted by TLR3 to the viral infection, causing the production of interferon β from the infected cell.
  2. Interferon β acts in an autocrine and paracrine mode to cause the production of interferon α and invoke an anti-viral state, leading to the degradation of dsRNA and inhibition of protein synthesis.

NK cells…

  1. Are activated by interferon α and interferon β produced by infected cells and activated macrophages.
  2. They are usually inhibited from killing normal cells by negative signals (e.g. MHC), but are now prompted to kill infected and damaged cells by positive activation signals.

Infected cells produce positive receptors for NK killing, leading to…

  1. Binding of the NK cell to the target cell.
  2. NK cell releases perforin by fusing membrane vesicles with the cell membrane.
  3. Perforin generates a pore in the cell membrane of the target cell, allowing granzymes to enter.
  4. Granzymes are a class of proteases that induce apoptosis, causing death of the target cell.

There was a question on my pathogenesis final today about an innate immune system effector present in mice and not humans, and I couldn’t remember the answer, so I drew a picture of a mouse and wrote “THANK CHEESES IT’S ONLY WORTH TWO POINTS!”

PMTH Morning Report: NK Cells

Good morning staff, zombies, and minions of Princeton Medbloro Teaching Hospital!

I am a baby medblr here, taking a stab at my first morning report. Today’s topic is…wait for it…my favorite cells…natural killer cells! Those bad ass little buggers whom you can thank your lucky stars for playing a role in keeping you a healthy, and relatively happy, humanoid. 

Give them credit because they truly are:

These lymphocytes don’t get as much credit as their ever so popular B and T cell counterparts, but don’t let the absence of genetic rearrangement deter your from what these gems do. They are a part of the innate immune system, and they are ready for action! Watch out infected cells, watch out neoplasms, NK cells are hunting you down!

How do you identify one of these super duper cells you ask? Well, lucky for us they are waving a giant flag. Thanks CD56! Of course, there are other markers but I like this one the best. Anyway, some NK cells let their CD56 shine more than others. What do I mean by that? You can see it with the use of our friend,flow cytometry!

But don’t think CD56 is all lonely on the surface…oh no. There’s a party going on. We have NKG2D getting all flirty with danger, and revving up the engines. All the while NKG2A is flirting’ with the HLA’s (Human Leukocyte Antigen) on cells passing by, and calming shit down. 

However, our party would not be complete without the KIRs (Killer Cell Immunoglobulin-Like Receptors) making everything more interesting. These aren’t generalists like NKG2D or NKG2A. Oh no, these dudes are picky. KIR2DL1 is looking for HLA-C2, KIR2DL2/3 is looking for HLA-C1, KIR3DL1 is looking for HLA-Bw4. But shhhh there’s a little secret that people don’t like to talk about…these KIRs can be frisky sometimes. I just listed the inhibitory KIRs, but substitute an S for the L (ex. KIR2DS1), and you’ve got yourself an activating KIR!

Yes, Yes, I know there is a lot of random information here. It’s important though because whether or not an NK cell kills, and how activated it is, depends on the BALANCE of those activating and inhibiting signals. 

Why do we give a shit about this? There are lot’s and lot’s of reasons, but I’ll list one. Tumor immunology! Turns out information about somebody’s HLA and KIR genotypes may be able to predict a patient’s response to immunotherapies, and maybe even outcomes in cancer patients. Pretty neat huh? 

Well, that’s all I’ve got. Be sure to grab coffee and an extra doughnut on your way out. 

Researchers discover neuroprotective role of immune cell

A type of immune cell widely believed to exacerbate chronic adult brain diseases, such as Alzheimer’s disease and multiple sclerosis (MS), can actually protect the brain from traumatic brain injury (TBI) and may slow the progression of neurodegenerative diseases, according to Cleveland Clinic research published today in the online journal Nature Communications.

The research team, led by Bruce Trapp, PhD, Chair of the Department of Neurosciences at Cleveland Clinic’s Lerner Research Institute, found that microglia can help synchronize brain firing, which protects the brain from TBI and may help alleviate chronic neurological diseases. They provided the most detailed study and visual evidence of the mechanisms involved in that protection.

“Our findings suggest the innate immune system helps protect the brain after injury or during chronic disease, and this role should be further studied,” Dr. Trapp said. “We could potentially harness the protective role of microglia to improve prognosis for patients with TBI and delay the progression of Alzheimer’s disease, MS, and stroke. The methods we developed will help us further understand mechanisms of neuroprotection.”

Microglias are primary responders to the brain after injury or during illness. While researchers have long believed that activated microglia cause harmful inflammation that destroys healthy brain cells, some speculate a more protective role. Dr. Trapp’s team used an advanced technique called 3D electron microscopy to visualize the activation of microglia and subsequent events in animal models.

They found that when chemically activated, microglia migrate to inhibitory synapses, connections between brain cells that slow the firing of impulses. They dislodge the synapse (called “synaptic stripping”), thereby increasing neuronal firing and leading to a cascade of events that enhance survival of brain cells.

Trapp is internationally known for his work on mechanisms of neurodegeneration and repair in multiple sclerosis. His past research has included investigation of the cause of neurological disability in MS patients, cellular mechanisms of brain repair in neurodegenerative diseases, and the molecular biology of myelination in the central and peripheral nervous systems.