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The Immune System Explained I – Bacteria Infection


The Immune System Explained I – Bacteria Infection

Every second of your life you are under attack. Bacteria, viruses, spores and more living stuff wants to enter your body and use its resources for itself. The immune system is a powerful army of cells that fights like a T-Rex on speed and sacrifices itself for your survival. Without it you would die in no time. This sounds simple but the reality is complex, beautiful and just awesome. An animation of the immune system.

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Why you are still alive - The immune system explained

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A pricked finger means the immune system is hard at work. An important part of the innate immune system, the skin – has been breached, and bacteria are entering the body. The first immune cells they encounter are mast cells and dendritic cells. These cells can distinguish self from non-self thanks to the recognition of pathogen-associated molecular patterns, or PAMPs, which are molecules associated with pathogens. This recognition is not specific to any invader, but rather identifies a general attribute common to pathogens. This recognition is thanks to their pattern recognition receptors, or PRRs. The PAMPs they recognize can include bacterial lipopolysaccharides. Now that microbial components have been recognized, the body springs into action, and the inflammatory response is initiated.
The mast cells stay on the battlefield, releasing histamine and heparin. Histamine causes vasodilation of nearby blood vessels and heparin is an anticoagulant. The result is increased blood flow to the infected area, which allows more white blood cells to get there. The mast cells also release cytokines, which are cell signalling proteins that affect the behaviour of nearby cells. In this case, the cytokines are used to call macrophages and neutrophils to the area.
Neutrophils are the most abundant white blood cells. They release cytokines as well, amplifying the inflammatory response. They attack pathogens in three ways – phagocytosis (engulfing pathogens – and they can ingest up to 20 each), degranulation (release of soluble antimicrobials), and the release of neutrophil extracellular traps, or NETs. NETs are primarily composed of the neutrophils’ DNA and bind pathogens. This binding occurs thanks to positive charged proteins on the bacteria’s surface interacting with negatively charged chromatin fibers.
Dendritic cells engulf antigens – foreign substances that elicit an immune response – and break them up into smaller pieces called epitopes. Dendritic cells in the epithelial tissue move out of t he infected area and into the lymph nodes.
The innate immune system has non-specific means of intruder identification and resistance. However, when the dendritic cells enter the lymph nodes, they link the innate immune system to the adaptive immune system. The adaptive immune system consists of T cells and B cells, and brings in anti-pathogenic weaponry specific to the attacker.
T-cells are produced in the thymus, differentiating into four types: helper T-cells, cytotoxic T-cells, regulatory T-cells, or Tregs, and memory T-cells.
T-cells are specific to one antigen. After leaving the thymus, they circulate the body until an APC presents an antigen that matches their T-cell receptor, or TCR. Following this initial activation, the T-cell’s CD4 or CD8 molecule also binds the MHC of the APC, stabilizing the connection. Helper T-cells and cytotoxic T-cells also need secondary signals, as well as cytokines to become fully activated. Following these signals, the T-cell begins to divide rapidly and moves to the site of inflammation to fight the pathogen. At the infection site, mast cells, neutrophils, and epithelial cells can produce cytokines to induce further activation and proliferation of the T-cells.
Immature B-cells can be activated either by attaching to a free-floating antigen or thanks to helper T-cells or dendritic cells that present an epitope matching their B-cell receptors, or BCRs. BCRs consist of a membrane bound antibody, which is a large, Y-shaped protein that bind antigens, CD79A and CD79B. The B-cell receptor and antigen undergo cell-mediated endocytosis.
Recognition of an antigen stimulates B-cells to proliferate, and the activated B-cells undergo clonal expansion. As they proliferate, these many clones undergo somatic hypermutation. AID introduces point mutations into the clones. For some clones, this results in an increased affinity to the antigen, while for others, this means a decreased affinity. The antigen is proteolytically broken down and an epitope is then displayed on the B-cell’s surface, attached to an MHC class II protein. Before the B-cell can do anything, a helper T cell with a complementary TCR, and CD4+ glycoprotein must bind the antigen. The T helper cell then releases cytokines that let the B-cell take the next step. This is a safety mechanism to prevent accidental activation of the B-cells. The B-cells that have decreased affinity then undergo apoptosis, while the B-cells with increased affinity differentiate, becoming either a plasma cell, or a memory B-cell. The plasma cells produce antibodies matching their BCRs into the blood and lymph. Meanwhile, the memory B cells store antibodies in case of future reinfection.
When antibodies bind antigens, they label them for destruction by cells such as macrophages and neutrophils. B-cells mediate your humoral immune response, so called because it involves substances in your body fluids.

The Immune System

This video describes the Immune System and explains how it detects and attacks any foreign organism that enters the body.

We learn how the team in the MRC Centre for Transplantation at King’s College London have developed a way to harness the power of the Immune System after a transplant, whilst maintaining the body’s capacity to resist infectious diseases.

Produced by Figment Productions.

Immune System - Fighting Infection by Clonal Selection

'Fighting Infection by Clonal Selection' was created to commemorate the 50th anniversary of Burnet's Clonal Selection Theory. The animation shows how clonal selection works during a bacterial infection of the throat. Frank Macfarlane Burnet was awarded the Nobel Prize in 1960 and is widely acknowledged as the founder of modern immunology.

View more biomedical animations at

Antibody Immune Response | Nucleus Medical Media

This 3D medical animation shows how antibodies stop harmful pathogens from attaching themselves to healthy cells in the blood stream. The animation begins by showing normal red and white blood cells flowing through the blood stream. Next, a single pathogen appears onscreen slowly moving toward its destination on the surface of a cell. The tubular extensions on the pathogen are surface proteins which attach to corresponding surface proteins on a white blood cell, or leukocyte. As the animation continues, more pathogens continue to attach to the white blood cell, rendering it ineffective.

During the immune system response, Y-shaped antibodies begin attacking the pathogen, binding to its surface proteins as the pathogen attempts to anchor to the blood cell. The antibodies completely block the pathogen from attaching to the blood cell, tagging the pathogen so that one of the immune system's leaner cells, a macrophage, appears onscreen to engulf and digest the pathogen.

Nucleus Medical Media is a leading creator and licensor of medical illustrations, animations, and interactive multimedia for: medical device and pharmaceutical companies; educational institutions; law firms; and hospitals. Learn more:


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- This video gives a great overview of the cells and functions of the immune system in response to a pathogen. Both the innate and adaptive immune system are explored. This video is a good starting point for the other Handwritten Tutorials Immunology videos. For more entirely FREE tutorials and accompanying PDFs visit

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Developed and produced for
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Professor Jacques Miller: T cells and the immune system

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Immune System: Innate and Adaptive Immunity Explained

The immune system (or immunity) can be divided into two types - innate and adaptive immunity. This video has an immune system animation. The innate immune system consists of defenses against infection that are activated instantly as a pathogen attacks. Adaptive immunity (or acquired immunity) is a subsystem of the immune system that contains highly specialised systemic cells and processes that kill pathogens and prevent their growth in the body. Innate vs adaptive immunity: it’s important to realize that innate and adaptive immunity are different. Their differences are explained in the video in layman terms.

Our immune system is a fascinating entity, that functions in quite a unique and efficient manner. Comprising of various types of cells, it is prepared for any kind of breach in the fortress of our body, and is equipped to fight off a staggering number of intruders.
In this video, we give you a brief overview of the immune system, and the basic types of cells involved, along with the function they carry out.

Each cell if the immune system carries out various roles, depending on the kind of threat the body is facing. However, they have certain basic roles which have been explained here.


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Immune response-Bacterial infections

Immunology topics

The Effects of Hyperglycemia on the Immune System

Developed and produced for a CME resource for physicians and healthcare providers.

Animation Description: Under normal circumstances, bacterial infection results in the release of chemokines that attract circulating neutrophils to the endothelium. This process is known as chemotaxis.

A variety of molecules are expressed on the endothelial cell surface that allow the neutrophil to be captured, then roll along the endothelium, then adhere.

Following adherence, the neutrophil migrates into the subendothelial tissue to reach the site of infection.

The neutrophil engulfs the bacteria and eliminates them via breakdown within the phagosomes — a process known as phagocytosis.

In states of hyperglycemia, chemotaxis is reduced. Adherence is also adversely affected.
Phagocytosis is also impaired by hyperglycemia.

Hyperglycemia also adversely affects the macrophage system. Under normal circumstances, circulating monocytes are attracted to sites of infection, roll, adhere, and then migrate into the subendothelial space. The monocyte then transforms into a macrophage.

which is then activated by cytokines released by the bacteria. The activated macrophage then engulfs the bacteria.

However, hyperglycemia results in decreased activation of macrophages, thereby arresting the process of macrophage phagocytosis of bacteria.

In addition to affecting neutrophil and macrophage function, hyperglycemia also affects the complement cascade. Under situations of normal glycemia, bacteria can activate the complement cascade.

Activation of the complement cascade results in the formation of transmembrane protein channels known as membrane attack complex (MAC) in bacterial membrane.

Membrane attack complexes make the bacterial membrane porous and the rapid influx of fluid results in the bacterial cell death.

Hyperglycemia inhibits the proper activation of the complement cascade, thereby reducing another pathway of the immune system.

Immune Response to Bacterial Infection (Basics to the Core)


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Brandl's Basics: Innate immune response to virus

This video introduces the key players of the immune system in response to a viral infection

The Immune System Explained I – Bacteria Infection online video cutter com

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